Quiz 2 Flashcards
Major centers of respiratory control in the brainstem
pneumotaxic
apneustic
Dorsal Respiratory Group (DRG)
Ventral Respiratory Group
Pneumotaxic center
provides inhibition to the dorsal respiratory group
acts as the “offswitch” for DRG
apneustic cneter
signals to the DRG that override the inhibition of the pneumotaxic center
therefore they prolong inspiration
- examples: sighing, yawning
Ventral respiratory group
active during FORCED respiratory efforts
-examples: coughing and sneezing
Dorsal Respiratory Group
group of active neurons during inSpiration
makes connection with the phreneric and intercostal nerves
Stretch receptors (Hering-Breur reflex)
lung receptor that sends inhibitory signals to the DRG
keeps you from taking too large of a breath
Irritant receptors
lung receptors that are stimulated by inhaled irritants
this protective mechanism increases respiratory rate and decreases the tidal volume (depth of breath) which causes you to pant.
-shallow, rapid breathing limits exposure to irritants
Juxtacapiallary receptors (J receptors)
lung receptors that are next to pulmonary capillaries
they are sensitive to congestion and excess fluid
decreases tidal volume (depth of breath)
reflex causes an increase in rapid breathing
How is breathing coordinated?
this autonomic and voluntary action had integration of afferent inputs to CNS respiratory centers and efferent output to repspiratory muscles
Peripheral chemoreceptors
found in the peripheral circulation in the aortic and carotid bodies
known as the O2 monitoring system and arterial H+ concentration
What is the negative feedback loop for peripheral chemoreceptors?
decreased in PO2 causes increased rate/depth of ventilation
vice-versa
increased PO2 causes decreased rate/depth of ventilation
central chemoreceptors
located near respiratory centers in the brainstem
responds directly to changes in arterial PCO2 only
directly sensitive to CSF [H+]
if PCO2 increases so does CSF [H+]
very sensitive to small changes in aterial PCO2
if you have increased [H+] then you have decreased pH
more CO2=more [H+} = more acidity
breathe more rapidly to get rid of CO2
Is CO2 lipid soluble?
YES, this allows it to cross the blood-brain barrier
What happens with obstructive lung disease?
the respiratory drive can be repressed therefore these individuals have trouble getting air out and so CO2 acccumulates
they have low O2 levels (hypoxcemic)
giving them supplemental O2 can help but we must be careful with creating the gradient
relationship between ventilation and arterial effects
greater ventilation when there is less arterial PO2
As PCO2 increases, ventilation INCREASES (linear)
ventilation increases as [H+] levels increase (linear)
Effect of progressively increasing exercise intensity
minute ventilation: linear increase until it reaches a break point for a larger slope during maximal effort
arterial PO2: a healthy person has sufficient O2 so there is no change during progressive increased in exercise
Arterial PCO2: constant decrease at low loads until it reaches a break point where it steeply decreases with increasing efforts; more ventilation to get rid of CO2
Arterial [H+]: increase only seen at high levels of work. As a result there is an increase of LA in the blood and an increased respiratory effort (hyperventilation)
Cheyne-Stokes breathing
seen in severe heart failure
gradual increase and decrease in depth of ventilation with a period of no breathing in between (apnea)
Apneustic breathing
pattern of deep sighs
brainstem damage produces this pattern of bigger, deeper and longer breaths
obstructive sleep apnea
structural issue; the soft tissue around the neck puts pressure on the upper airways and causes compression and loss of breath
apnea=”not breathing”
closing of the pharynx during inspiration and arousal by respiratory drive
associated with obesity
treatment of a breathing apparatus which uses positive pressure to splint the airways open
-Continuous Positive Airway Pressure
Restrictive disease
VOLUME limitation
“belt around the lungs”
decreased FVC and FEV1
Obstructive disease
FLOW limitation
decreased airway diameter
problematic during expiration
normal or decreased FVC and extremely decreased FEV1
Obstructive Flow-Volume Loop
limitation of FLOW so that the peak flow rate drops rapidly
Restrictive Flow-Volume Loop
shape of the loop is the same but much smaller
Obstructive diseases
obstruction to FLOW
COPD-chronic obstructive pulmonary disease
includes chronic bronchitis, emphysema, asthma
symptoms of obstructive diseases
chronic cough
coughing out of mucus
wheexing
dyspnea with exertion
Pathology in obstructive disease
inflammation of lining of smaller airways
increased mucus production or impaired clearance
impaired cilia in conducting zone leads to less filtration
mucosal thickening
bronchial smooth muscle spasm leads to further narrowing of the airways and increased resistance
seen in people with asthma
tissue destruction; the elastic tissue is lost which decreases SA and gas exchange
seen in people with empheysema
effects on lung function with obstructive
loss of elastic recoil; overly compliant airways that can inflate but can’t deflate
this causes hyperinflation(air trapping) and “barrel chest”
tendency for airway collapse from dynamic compression
loss of alveolar surface area
poor oxygen delivery and CO2 clearance(hypercapnia)
creates vasoconstriction with poor ventilation
resulting in right sided heart failure=cor pulmonale
chronic bronchitis
inflammation of bronchi
caused by irritants such as smoking
sputum-producing cough
ciliary dysfunction with increased mucous glands
Emphysema
destruction of alveoli
results in poor gas exchange
feels like taking sips of air on full inhaled lungs
expends a lot of energy to breath
they have a mechanically inefficient diaphragm that can’t generate enough force for breathing
Emphysema treatment
smoking cessation medications- inhaled corticosteroids, anticholinergics, B2 agonsits oxygen therapy surgery pulmonary rehab- helps manage symptoms
Asthma
reversible obstruction
excess mucus, edema and inappropriate activation of bronchiole SM creating a narrowed airway
worse with environmental factors
-dust, pollen, cold air
three kinds of COPD
emphysema
chronic bronchitits
airway hyperactivity (constricts and further creates obstruction)
Corticosteroids
useful in asthma
powerful anti-inflammatories
flovent
sympathomimetics
epinephrine adn ephedrine are non-selective
peripheral vasoconstriction and tachycardia in addition to bronchodilation
selective B2 agonists are ideal
Albuterol
parasympatholytics
anticholinergics
usually used in COPD; emphysema
Spiriva
bronchiectasis
result of infection
cystic fibrosis
occurs int he pancreas lung consequences occurs in much younger- teens to 20s OBSTRUCTIVE lung disorder inherited autosomal recessive pulmonary secretions are thick
Restrictive Lung Dysfunction
VOLUME limitation
disorder of compliance; issues with inflating
all lung volumes and capacities are decreased
harder to breath
Causes of RLD
pregnancy- difficulty inspiring with limited diaphargm movement stroke- causes neuromuscular weakness obesity arthritis- limited lung volume capacity immunologic nutritional and metabolic issues trauma connective tissues issues cardiovascular/pulmonary issues
long bone structure
periosteum —> endosteum —> bone marrow
diaphysis
the shaft of the long bone
yellow bone marrow
contains fat
no RBC production
epiphysis
end of the bones
made up of spongy bone (callcaneous)
metaphysis
region between the shaft and the epiphyses
contains the epiphyseal growth plate
widens as it approaches the epiphysis
what does the marrow cavity contain?
found in the center of the shaft it contains marrow
what is the diaphysis composed of?
a peripheral layer of compact bone called the bone collar
the central part is hollow and called the medullary cavity
what does the medullary cavity contain?
either red or yellow bone marrow that contains hematopoetic tissue capable of producing red and white blood cells
where is cancellous (spongy bone) found?
in the epiphysis and distal portions of the shaft of the long bones