Download Semester 2 Case 1: The Stabbing

Semester 2
Case 1: The Stabbing
• What are the mechanics of breathing?
[1] Movement
of air into and out of the lungs takes place because of pressure differences
caused by changes in lung volumes. Air flows from a high-pressure area to a low-pressure
area. The changes in volume in the lungs occur through the contraction of skeletal muscles
– those that insert on the ribcage & the diaphragm. When the muscles elevate the ribs, they
swing outward, increasing the depth of the thoracic cavity.
Normal breathing at rest  Uses diaphragm & external intercostals muscles.
Increased depth & frequency of breathing  In addition, uses accessory respiratory muscles,
which are: internal intercostals, sternocleidomastoid, serratus anterior, pectoralis minor,
scalene, transversus thoracis, transversus abdominis, external & internal oblique, and rectus
abdominis muscles.
Inhalation is ALWAYS ACTIVE. The diaphragm contracts, flattening to the floor of the
thoracic cavity & increasing its volume. External intercostal muscles contract, elevating ribs.
Accessory respiratory muscles can assist by increasing speed + amount of rib elevation.
Exhalation CAN BE ACTIVE OR PASSIVE. Passive occurs via elastic recoil of lungs. When
active, internal intercostals + transversus thoracis muscles depress ribs. Abdominal muscles
can assist by compressing the abdomen & forcing the diaphragm upward.
Quiet Breathing (Eupnea)
Inhalation involves muscular contractions, but exhalation is passive. Deep breathing relies
more on the diaphragm, whereas shallow breathing relies more on the intercostal muscles.
Expansion of lungs stretches their elastic fibers. Elevation of rib cage stretches opposing
skeletal muscles & elastic fibers in the connective tissues of the body wall. When muscles of
inhalation relax, elastic components recoil – AKA. Elastic rebound!
Forced Breathing (Hyperpnea)
Inspiration and exhalation are both active. Accessory muscles assist with inhalation &
exhalation also involves the contraction of internal intercostal muscles. Abdominal muscles
are also used at maximum levels of forced breathing.
Normal adult respiratory rate = 12-18 per minute.
Normal child respiratory rate = 18-20 per minute.
• What are the different respiratory volumes?
- Respiratory Minute Volume, VE = Respiratory rate, ƒ X Tidal Volume, VT.
Measures pulmonary ventilation. Average at rest = 12 x 500ml = 6.0 litres per minute.
- Alveolar Ventilation, VA = Respiratory rate, ƒ X(Tidal volume, VT – Anatomic Dead
Space, VD).
The amount of air reaching the alveoli, and hence participating in gas exchange, each
minute. Anatomic dead space is the volume of air left in the conducting passages. Average
VA at rest = 12 x (500ml – 150ml) = 4.2litres per minute.
Pulmonary volumes include:
- Resting Tidal Volume, VT: The amount of air you move into & out of your lungs during
a single respiratory cycle under resting conditions. Average = 500ml.
- Expiratory Reserve Volume, ERV: The amount of air you can voluntarily expel after
you have completed a normal, quiet respiratory cycle. (i.e. additional air using
accessory muscles. Average in males = Additional 1l, in females = 700ml).
- Residual Volume: Amount of air remaining in lungs after a maximal exhalation.
Average in males = 1200ml, and females = 1100ml).
- Minimal Volume: Amount of air that would remain in the lungs if they were allowed to
collapse. Ranges from 30-120ml. Cannot be measured in a healthy person. The
reason some air is still present even after lung collapse is because surfactant coating
the alveolar surfaces prevents their collapse.
-
Inspiratory Reserve Volume, IRV: Amount of air you can take in over & above the
tidal volume. Average in males = 3300ml, females = 1900ml.
Respiratory capacities can be calculated using the pulmonary volumes:
- Inspiratory Capacity = Tidal volume, VT + Inspiratory Reserve Volume, IRV. It is the
amount of air that can be drawn into the lungs after a quiet respiratory cycle.
- Functional Residual Capacity, FRC = Expiratory Reserve Volume, ERV + Residual
Volume. It is the amount of air in the lungs after a complete quiet respiratory cycle.
- Vital Capacity = Expiratory Reserve Volume, ERV + Tidal Volume, VT + Inspiratory
Reserve Volume, IRV. It is the maximum amount of air that can be moved into & out
of the lungs in a single respiratory cycle. Average in males = 4800ml, females =
3400ml.
- Total Lung Capacity = Vital Capacity + Residual Volume. Average in males = 6l, in
females = 4.2l.
• How is respiration controlled?
Under normal conditions, cellular rates of absorption of O2 and generation of CO2 = Capillary
rates of delivery of O2 and removal of CO2 = Rate of O2 absorption and CO2 excretion at
lungs.
If this becomes unbalanced, homeostatic mechanisms restore equilibrium by: changes in
bloodflow & oxygen delivery at the local level, and changes in depth & rate of respiration via
the brain’s respiratory centres.
Changes in respiratory centres are coordinated with changes in cardiovascular function. E.g.
-fluctuations in blood pressure & cardiac output.
At Local Level:
When a peripheral tissue becomes more active, interstitial O2 pressure falls & CO2 pressure
rises. Therefore, more oxygen is delivered and more carbon dioxide is carried away. Rising
CO2 pressure levels causes relaxation of smooth muscles in walls of arterioles & capillaries
in the area, increasing local bloodflow.
Local factors also influence blood flow to alveoli (lung perfusion) with alveolar ventilation.
Alveolar capillaries constrict when O2 pressure is low, so directing blood towards high O2
pressures. Also, when CO2 pressure increases, bronchioles increase in diameter
(bronchodilation), directing airflow to bronchioles that have high CO2 pressure - improves
efficiency of gas transport.
At Respiratory Centres In The Brain:
[1,2] Involuntary centres regulate activity of respiratory muscles & control Respiratory Minute
Volume by adjusting frequency and depth of pulmonary ventilation.
Voluntary centres affect either the output of the respiratory centres in the medulla oblongata
& pons OR the output of motor neurons in the spinal cord that control respiratory muscles.
The respiratory rhythmicity centre is made up of several groups of neurons located bilaterally
in the medulla oblongata:
* Dorsal Respiratory Group (DRG): Located in dorsal part of the medulla, mostly in the
nucleus of the tractus solitarius. Functions in every respiratory cycle. Causes inspiration. It
contains neurons that control lower motor neurons innervating external intercostals & the
diaphragm.
* Ventral Respiratory Group (VRG): Located in ventral part of the medulla. Functions only
during forced breathing. It has an expiratory centre consisting of neurons that innervate
lower motor neurons controlling accessory respiratory muscles involved in active inhalation.
Its Inspiratory centre contains neurons involved in maximal inhalation.
When inspiratory neurons are active, expiratory neurons are inhibited, and vice versa.
During quiet breathing:
1) DRG activity ↑ for 2 seconds. This stimulates the diaphragm and external intercostal
muscles via ramp signals & inhalation occurs.
2) DRG neurons then become inactive for 3 seconds, whilst inspiratory muscles relax.
Passive exhalation occurs.
During forced breathing:
1) DRG and the VRG inspiratory centre are active, but expiratory centre of VRG is
inhibited. This stimulates the diaphragm, external intercostal muscles, & accessory
muscles. Inhalation occurs.
2) DRG and inspiratory centre of the VRG are inhibited. VRG expiratory centre is
activated. This stimulates the appropriate accessory muscles, and active exhalation
occurs.
The apneustic centres & pneumotaxic centres of the pons are paired nuclei that adjust
the output of the respiratory rhythmicity centres in the medulla oblongata. These 2 centres
regulate respiratory rate and the depth of respiration in response to sensory stimuli or input
from other centres in the brain.
Each APNEUSTIC centre provides continuous stimulation to the DRG on that side of the
brain stem. In normal breathing, they stimulate increased intensity of inhalation over 2
seconds. Then, the PNEUMOTAXIC centre on each side inhibits that apneustic centre.
During forced breathing, apneustic centres are also provided with sensory input regarding
amount of lung inflation by the vagus nerves.
Pneumotaxic centres inhibit apneustic centres & promote passive or active exhalation.
Activity of pneumotaxic centres is affected by the hypothalamus, cerebrum, respiratory rate
& depth. They modify the pace of respiration:
↑ pneumotaxic output  Shortens duration of each inhalation, so quickens pace of
respiration.
↓ pneumotaxic output  Slows respiratory pace  Increases depth of respiration because
apneustic centres are more active.
Respiratory Reflexes:
Activities of respiratory centres are modified by sensory information from several sources:
•
Chemoreceptors sensitive to partial pressures of O2 and CO2, or pH of the blood or
cerebrospinal fluid.
• Baroreceptors in aortic & carotid sinuses sensitive to changes in blood pressure.
Respiratory rate increases when blood pressure falls. This is stimulated by the vagus
& glossopharyngeal nerves.
• Stretch receptors in lungs that respond to changes in volume via vagus nerves to the
DRG. (Hering-Breuer inflation reflex)
• Irritating physical or chemical stimuli in the nasal cavity, larynx, or bronchial tree.
• “J receptors” in alveolar walls are stimulated when pulmonary capillaries become
engorged with blood or when pulmonary oedema occurs. Can give a person the
feeling of dyspnoea.
• Other sensations, including pain, changes in body temperature, & abnormal visceral
sensations.
Central Chemoreceptors – A chemosensitive area in the ventrolateral surface of the medulla
oblongata responds to PCO2 and pH of the blood and CSF. CO2 reacts with water in tissues,
forming carbonic acid (H2CO3), which dissociates into H+ and HCO3-. The H+ ions then have a
direct stimulatory effect on respiration. Blood CO2 has a more potent effect in stimulating
chemoreceptors, as the blood-brain barrier isn’t very permeable to H+, but is to CO2.
Peripheral Chemoreceptors – Most chemoreceptors are located in the carotid bodies, which
are located bilaterally in the bifurcations of the common carotid arteries. Information is
carried from carotid chemoreceptors via the glossopharyngeal nerve (cranial nerve IX) to the
DRG. There are also a few chemoreceptors in the aortic bodies, which are located along the
arch of the aorta. Information is carried from aortic chemoreceptors via the vagus nerve
(cranial nerve X) to the DRG. Peripheral chemoreceptors are strongly stimulated by changes
in PO2, and to a lesser extent changes in PCO2 and pH.
Stimulation of chemoreceptors causes increased depth & rate of respiration.
Voluntary Control of Respiration
Activity of cerebral cortex has an indirect effect on respiratory centres, as the following
examples show:
• Conscious thought processes tied to strong emotions stimulate centres in
hypothalamus.
• Emotional states can affect respiration through activation of sympathetic nervous
system (bronchodilation – increases respiratory rate) or parasympathetic nervous
system (bronchoconstriction – decreases respiratory rate).
• Anticipation of strenuous exercise can trigger automatic increase in respiratory rate,
along with increased cardiac output, by sympathetic stimulation.
[3] Pleural Pressure
Elastic recoil of lungs is exactly balanced by the elastic recoil of the chest wall trying to
expand the chest. These 2 opposing forces create a subatmospheric (relatively negative)
pressure within the intrapleural space. (When air is in the alveoli, intrapleural pressure is
also less than the pressure inside the lungs). Intrapleural pressure fluctuates during
breathing, but is about -0.5kPa at the end of quiet expiration. This gradient is known as the
TRANSMURAL or TRANSPULMONARY PRESSURE. This pressure ensures that the lungs
are held partially expanded in the thorax. It links the lungs (which are like suspended
balloons) with the chest wall.
Alveolar Pressure
This is the pressure of the air inside the lung alveoli. When the glottis is open and no air is
flowing into or out of the lungs, the pressures in all parts of the respiratory tree are equal to
atmospheric pressure. To cause inward flow of air into the alveoli during inspiration, the
pressure in the alveoli must fall to a value slightly below atmospheric pressure.
Lung Compliance
This is the extent to which the lungs will
expand for each unit increase in
transpulmonary pressure. This picture
shows the graph of lung compliance for a
healthy person. The characteristics of the
compliance diagram are determined by the
elastic forces of the lungs. This can be
divided into: the elastic forces of the lung
tissue itself (elastin & collagen), and elastic
forces caused by surface tension of the
fluid (surfactant) that lines the inside walls
of the alveoli and other lung spaces.
Surfactant & Surface Tension
When water forms a surface with air, the
water molecules on the surface develop a
very strong attraction towards one another.
On the inner surfaces of the alveoli, the same occurs and tries to make the alveoli collapse,
forcing air into the bronchial tree. The net effect of this is to cause an elastic contractile force
of the entire lungs. Surfactant is a surface active agent in water, which means that it greatly
reduces the surface tension of water. It is secreted by Type II alveolar epithelial cells.
Surfactant is a mixture of several phospholipids, proteins, & ions, the most important of
which are dipalmitoylphosphatidylcholine, surfactant apoproteins, and calcium ions. The
phospholipids are responsible for reducing surface tension, by not dissolving uniformly in the
fluid lining the alveolar surface. Surfactant therefore reduces the effort required by the
respiratory muscles to expand the lungs.
During inspiration, intrathoracic volume increases, which lowers intrapleural pressure,
making it more negative. This causes the lungs to expand & air to enter.
During expiration, muscles of the chest wall relax. Lungs return to their original size by
elastic recoil, expulsing air.
In quiet breathing, intrapleural pressure is always negative.
In forced breathing, intrapleural pressure is positive, forcing a reduction in lung volume with
the expulsion of air.
Intrapleural pressure is more negative at lung apices than at the bases as the bases are
more compressed.
• How should a normal chest X-ray look?
[4] Tissues
that are very dense (RADIOPAQUE) absorb many of the x-rays & appear whiter
on the film. Tissues that are less dense (RADIOLUCENT) let more x-rays pass through & the
image appears darker.
- Gas/Air = Black
- Fat = Dark Gray
- Soft tissues/Water = Light gray
- Bone = Off-white
- Metal/Contrast material = Bright white
There are 2 types of frontal chest radiographs: PA and AP.
The PA x-ray provides optimal view & is the view of choice. Patient stands with anterior
aspect of chest against the film cassette. Exposure is then taken in full inspiration with the xray source located 2 metres behind the patient.
An AP view is obtained when the patient requires an ongoing assessment, resuscitation,
treatment, or monitoring. The patient either sits or lies on a trolley. An AP x-ray
distorts/enlarges the heart due to magnification.