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For Air to enter the lungs during inhalation the pressure must drop below 760 mmHg
The pressure inside the lungs must drop below this level
Inspiration at rest
Begins when the diaphragm contacts and flattens and the external intercostal muscles contract, lifting the rib cage
As the volume of the lungs increases
The intrapulmonary pressure drops below atmospheric pressure and air flows into the lungs
Expiration at rest is a passive process
It relies on the elastic recoil of the lungs
Once the diaphragm and external intercostals relax, the thoracic cavity returns to its resting size
As lung volume decreases
Intrapulmonary pressure rises above atmospheric pressure and air flows out of the lungs
Forced inspiration
Involves a greater contraction of the diaphragm and external intercostals and may recruit accessory muscles such as the SCM and scalenes
These efforts further expand the throacic cavity and create a larger drop in intrapulmonary pressure
Forced expiration
Becomes an active process where the internal intercostals and abdominal muscles contract to forcefully decrease thoracic volume and expel more air from the lungs than elastic recoil alone can achieve
Emphysema
In pts with this the elastic fibers of the lungs are damaged, reducing the lungs ability to recoil during expiration
This makes passive expiration less efficient, leading to air trapping, increased residual volume, and the characteristic barrel chest appearence
Restrictive lung disease
With this lung tissue becomes stiff or scarred, reducing lung compliance
As a result inspiration becomes more difficult even though expiration may remain relatively normal
These pts often take rapid shallow breaths to reduce the work of breathing
Neuromuscular disorders
Diseases that affect the diaphragm or intercostal muscles can impair both inspiration and expiration
In ALS for example the loss of motor neurons weakens the diaphragm leading to hypoventilation, reduced lung volumes and eventually respiratory failure
Ventilation-perfusion, V/Q
Refers to the relationship between the air that reaches the alveoli via pulmonary capillaries
Average V/Q ratio in the lungs at rest
0.8
Low V/Q
Indicates poor ventilation relative to perfusion
High V/Q
Suggests adequate ventilation but poor perfusion
Hypoxic pulmonary vasoconstriction
Areas of the lung that are poorly ventilated will experience vasoconstriction of the pulmonary arterioles to divert blood to better ventilated regions
Pulmonary embolism
Blood clot blocks perfusion to parts of the lung
Ventilation may be normal but perfusion is absent
This causes a high V/Q mismatch aka dead space ventilation
COPD
Mucus and inflammation obstruct airflow to the alveoli, creating areas where perfusion is intact but ventilation is impaired
A low V/Q mismatch, aka shunt like state
Pneumonia
Fluid or exudate in the alveoli prevents normal ventilation
Even though blood continues to flow through the capillaries, gas exchange is impaired, another low V/Q situation
Oxygenated is transported in the blood in two forms
Bound to hemoglobin
Dissolved in plasma
Carbon dioxide is transported in the blood in three forms
As bicarb
Bound to hemoglobin
Dissolved in plasma
Anemia
There is reduced hemoglobin available to bind to oxygen even if PaO2 is normal
Oxygen hemoglobin dissociation curve
Illustrates the relationship between the partial pressure of oxygen and the percentage of hemoglobin saturated with oxygen
How the oxygen hemoglobin saturation curve works
In the tissues where PaO2 is lower, hemoglobin releases oxygen to meet metabolic demands (so that oxygen can be used by the tissues that need it like skeletal muscles)
A rightward shift (reduced affinity for oxygen, more unloading tissues)
Is caused by increased temperature, increased CO2, decreased pH, and increased 2,3 BPG
Benefit of a rightward shift
Helpful during exercise or in metabolically active tissues because it allows more oxygen to be released from hemoglobin and used by the tissues for metabolism
A leftward shift
Occurs with decreased CO2, increased pH, and decreased temperature
Exercise and fever (rightward shift)
The curve shifts to the right
This promotes oxygen unloading at tissues, helping meet metabolic demand
Hypothermia or alkalosis (leftward shift)
Curve shifts to the left, meaning hemoglobin holds onto oxygen more tightly
Supplemental O2 indication
Hypoxemia
Short AND long acting beta 2 agonist inhaler indication
Airway obstruction
Inhaled corticosteroids indication
Airway inflammation and obstruction
Muscarinic antagonists
Airway obstruction
PT implications/possible adverse side effects of supplemental O2
Long term use may cause cytotoxic damage and depression of ventilation
Short acting beta 2 agonist inhaler mechanism of action
stimulate the B-2 receptors in smooth muscle cells that line the bronchi, thus causing relaxation and dilation of the airways
These medications act quickly and are used to relief from sudden attacks/symptoms
Long acting beta 2 agonist inhaler mechanism of action
stimulate the B-2 receptors in smooth muscle cells that line the bronchi, thus causing relaxation and dilation of the airways
Are longer acting and are used regularly in chronic asthma and COPD
Inhaled corticosteroids mechanism of action
suppress airway inflammation
They also enhance B-2 adrenergic receptor expression and function and are often used with LABAs in the treatment of airway obstruction
Muscarinic antagonists mechanism of action
Activate bronchoconstriction therefore inhibiting this mechanism causes bronchodilation
PT implications/possible adverse side effects of short and long acting beta 2 agonist inhaler
Increased sympathetic activation and HR
PT implications/possible adverse side effects Of inhaled corticosteroids
At high doses they may increase the risk of HTN, hyperlipidemia, and glucose intolerance
PT implications/possible adverse side effects Of muscarinic agents
dry mouth/skin
Headache
Confusion
Dizziness
Tachycardia
Blurred vision
Delirium
Decreased GI activity