Pulmonary Pt2 Flashcards
Where does the normal automatic process of breathing originate from?
The Brainstem
Neurons in which part of the brain control unconscious breathing?
Neurons in the medulla and pons in the brainstem
If voluntary control of breathing is needed, which part of the brain can override the medulla and pons?
The cortex
The automatic rhythm of breathing is controlled by neurons located where?
In the Respiratory nuclei of the medulla rhthymicity center.
inspiratory center
-(dorsal respiratory group)
•frequent signals, you inhale deeply
•signals of longer duration, breath is prolonged
expiratory center
(ventral respiratory group)
•involved in forced respiration
rate and depth control
Pons
pneumotaxic center (pons)
•sends inhibitory impulses to inspiratory center, as impulse frequency rises, breaths shorter, faster and shallower (turns of inspiration to prevent overinflation of lungs)
_______ is the reticular formation of the medulla beneath the floor of the fourth ventricle
medullary respiratory center
apneustic center (pons)
•promotes maximal lung inflation and long, deep breaths of Inspiration and expiration (turns off the pneumotaxic
Dorsal Respiratory Group (medullary resp center)
sets the basic respiratory rhythm
Ventral Respiratory Group (medullary resp center)
associated with forced respiration
Dorsal and Ventral Respiratory Groups’ cells have/responsible
•intrinsic periodic firing abilities and are responsible for basic rhythm of ventilation
Pre-Botzinger Complex (medullary resp center)
-(part of Ventral Group) = essential for generation of the respiratory rhythm
T/F Dorsal and Ventral Respiratory Groups’ cells, even when all afferent stimuli is abolished, these cells generate repetitive action potentials that send impulses to the diaphragm and other respiratory muscles
True
pneumotaxic center location/inhibits/limits
- located in upper pons
- inhibits inspiration
- limits the burst of action potentials in the phrenic nerve, effectively decrease the tidal volume and regulating the respiratory rate
Impulses from ____ and _____ modulate the output of inspiratory cells
the Vagus (X) and Glossopharyngeal (IX)
Input to Respiratory Centers from limbic system and hypothalamus
resp effects of pain and emotion
Input to Respiratory Centers from chemoreceptors
Resp effects of blood pH, CO2 and O2 levels
•Rate and depth of breathing adjusted to maintain levels of:
- pH
- Pco2
- Po2
what can exist in absence of pneumotaxic center
-“Fine tuning” of respiratory rhythm because a normal rhythm can exist in the absence of this center
primary stimulus for central chemoreceptors
pH of CSF
Apneustic center location/impulse/promotes/sends
- located in the lower pons
- Impulses have an excitatory effect on the Dorsal Respiratory Group in the medulla
- Promotes inspiration
- Sends signals to the Dorsal Respiratory Group in the medulla to delay the “switch off” signal provided by the pneumotaxic center
CO2 easily crosses
BBB
in CSF the CO2 reacts with water and releases
H+
the cycle of inspiration:
-Crescendo of action potentials leading to a ramp of strengthening inspiratory muscles
-
-Inspiration action potentials cease and inspiratory muscle tone falls
-
-Expiration occurs due to elastic recoil of lung tissues and chest wall
central chemoreceptors strongly stimulate
inspiratory center
“blowing off” CO2 pushes reaction to the
left
Input to Respiratory Centers from airways and lungs
and lungs
-irritant receptors in respiratory mucosa
•stimulate vagal signals to medulla, result in bronchoconstriction / coughing
-stretch receptors in airways - inflation reflex
•excessive inflation triggers stop of inspiration
•J-receptors - juxtapulmonary capillary receptors - increase rapid, shallow breathing
hypoventilation pushes reaction to the
right
ketoacidosis may be compensated for by _____ respirations
Kussmaul
peripheral chemoreceptors
-found in major blood vessels
>aortic bodies (signals medulla via C.N. X)
>carotid bodies (signal medulla by C.N. IX)
central chemoreceptors
-in medulla
>primarily monitor pH of CSF
>inc H+ stimulates ventilation
>dec H+ inhibits it
central chemoreceptors mediate ___ % of ventilatory response
80%
peripheral chemoreceptors mediate ____ % of ventilatory response
20%
normal pH of CSF
7.33
CSF has much less buffering capacity compared to blood, resulting in:
greater change in pH with changes in PCO2
•With _______ disease, the hypoxic drive to ventilation becomes very important
severe lung disease
most important peripheral chemoreceptors
carotid bodies
carotid bodies afferent nerve
glossopharyngeal (C.N. IX)
Carotid bodies respond to
decreases in arterial PO2 and pH, and increases in arterial PCO2
carotid receptors respond to drop in ___ via ___ nerve
pH and C.N IX
aortic receptors respond to ____ via ____ nerve
PCO2 and C.N. X
ventilation receptors enhance by:
1) metabolic acidosis
2) low PO2 (<60 mmHg)
3) elevated temperature
ventilation receptors suppressed by:
1) metabolic alkalosis
2) any CNS depressant
3) cold
4) narcotics
•Changes can be compensated by ______ of HCO3- into the CSF
- active transport
- Example: A patient with chronic lung disease will have CO2 retention, but may have a near normal CSF pH and a resulting low ventilation for his or her PCO2 level
Transitional flow
a mixture of laminar and turbulent flow and occurs at branch points in the airways
The trachea and larger airways have either
•turbulent or transitional airflow
peripheral chemoreceptors located
-Located in the carotid bodies at the bifurcation of the common carotid arteries, and in the aortic bodies above the aortic arch
Laminar flow in
smallest airways
Intrapleural Pressure
Pressure in the potential space between the parietal and visceral pleura is normally subatmospheric around -3 to -5 cm H2O
T/F Not all alveoli are ventilated equally
True
Alveoli in the lower lungs (base) receive
•receive more ventilation per breath than alveoli of the upper regions of the lungs in the awake, spontaneously breathing, upright patient.
dependency
•The influence of gravity on a supported structure
-accounts for regional differences in alveolar ventilation (dependent vs. nondependent)
difference in volume and compliance leads
leads to a difference in ventilation
Effective gas exchange depends on
•depends on an approximately even distribution of gas (ventilation) and blood (perfusion) in all portions of the lungs (VQ).
Ventilation and perfusion depend
body position
Distribution of perfusion in the pulmonary circulation also is affected by
alveolar pressure (gas pressure in the alveoli)
determine rate of diffusion of each gas and gas exchange between blood and alveolus
partial pressures (as well as solubility of gas)
the volume remaining in the lungs at the end of a normal tidal expiration.
FRC (functional residual capacity)
Elasticity
•the tendency of lung tissue to return to its original (or relaxed) position after an applied force has been removed.
to keep the lungs inflated what is required and how is it provided
- an opposing pressure
- Provided by the chest wall and the respiratory muscles (Compliance)
end of expiration diaphragm is
relaxed
inspiration diaphragm is
contracting
end of inspiration diaphragm
contracted
expiration diaphragm
relaxing
Lungs do what with negative pressure in the thorax
expand
small airway closure and trapping somewhat prevents air ____
loss
West Lung Zones
- PA = alveolar pressure
- Pa = arterial pressure
- Pv = venous pressure
- Zone I: PA>Pa>Pv
- Zone II: Pa>PA>Pv
- Zone III: Pa>Pv>PA
- Zone I = PA, compressed arterioles = V w/o Q = deadspace (usually only seen in mechanically ventilated pts)
Airway collapse during forced expiration
in normal individuals this only occurs in very small airways overall result is that the lungs cannot be completely emptied
compliance is the opposite of
elasticity
compliance
it is a measure of the distensibility of the lung
Minute Ventilation (VE) equation
Ve = Vt x f
VE = minute ventilation (volume per minute) vT = tidal volume (volume per breath) f = frequency or RR (Respiratory Rate) Example: VE = vT x f = 500 x 10 = 5000 ml/min.
anatomic ds =
conducting airway
mechanical ds =
ventilator machine circuit, ET tube, etc
alveolar ds =
nonperfused alveoli
physiologic ds =
the sum of anatomic & alveolar ds
•If you want to increase alveolar ventilation, should you increase respiratory rate or tidal volume?
increasing tidal volume is more effective to increase VA than increasing breathing frequency
Increasing frequency while maintaining a constant volume results in
§in proportional increase of both alveolar ventilation and dead space
Increasing tidal volume while maintaining constant frequency results in
§no change to dead space but an increase in alveolar ventilation
what is important for gas exchange between air in lungs and blood in capillaries
air-water interface
Time required for gases to equilibrate
0.25 sec
RBC transit time at rest
0.75 sec to pass through alveolar capillary
•Reduced compliance is caused by:
- Increased fibrous tissue (ex. pulmonary fibrosis)
- Alveolar edema
- If the lung remains unventilated for a long period with low volumes (atelectasis and increases in surface tension)
RBC transit time with vigorous exercise
- Diameter of airway
- Flow (Laminar vs. Turbulent)
- Density of gas (viscosity)
- Governed by Poiseuille’s Law
- Age or Pathologies that affect recoil (ex. Pulmonary fibrosis)
% of O2 bound to hemoglobin
98.5%
% of O2 dissolved
1.5%
Alveolar minute ventilation equation
VA = (VT - VDS) x RR
VA = alveolar ventilation VT = tidal volume VDS = physiologic dead space ~ 1ml per pound ideal body wgt. Example: 150 pound pt. VA = (VT - vDS ) x RR = (500 - 150) x 10 = 3500 ml/min.
alveolar age effects
•Decreased alveolar elasticity and lung compliance, respiratory muscles weaken
•Higher Residual Volume and decreased maximal expiratory flow rates
-
•Loss of alveolar surface area
•Decreased pulmonary perfusion
•Restrictive disorders
- decrease compliance and vital capacity •Pulmonary Fibrosis •Sarcoidosis •Interstitial Lung Disease •Myasthenia gravis •ALS
•Obstructive disorders
-interfere with airflow, expiration requires more effort or is less complete
•Asthma
•COPD
•Emphysema
Mixture of gases; each contributes its
•partial pressure
-at sea level 1 atm. of pressure = 760 mmHg
-nitrogen constitutes 78.6% of the atmosphere so
•PN2 = 78.6% x 760 mmHg = 597 mmHg
•PO2 = 159
•PH2O = 3.7
•PCO2 = + 0.3
•PN2 + PO2 + PH2O + PCO2 = 760 mmHg
•Partial pressures (as well as solubility of gas) determine
-determine rate of diffusion of each gas and gas exchange between blood and alveolus
alveolar air
-humidified, exchanges gases with blood, mixes with residual air
-contains:
•PN2 = 569
•PO2 = 104
•PH2O = 47
•PCO2 = 40 mmHg
•Henry’s law
-amount of gas that dissolves in water is determined by its solubility in water and its partial pressure in air
factors affecting gas exchange
•Concentration gradients of gases
-PO2 = 105 in alveolar air versus 40 in blood
-PCO2 = 45 in blood arriving versus 40 in alveolar air
•Gas solubility
-CO2 20 times as soluble as O2
•O2 has conc. gradient, CO2 has solubility
•Membrane thickness - only 0.5 mm thick
•Membrane surface area - 100 ml blood in alveolar capillaries, spread over 70 m2
•Ventilation-perfusion coupling - areas of good ventilation need good perfusion
Oxygen concentration in arterial blood
-20 ml/dl
•Oxyhemoglobin dissociation curve
- relationship between hemoglobin saturation and PO2 is not a simple linear one
- after binding with O2, hemoglobin changes shape to facilitate further uptake (positive feedback cycle)
