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Vital sign respiration



Anatomy and Physiology


The Mechanics of Breathing

intercostal mDuring inspiration, the external uscles contract, lifting the lower ribs up and out. The diaphragm moves down, increasing the volume of the pleural cavity. Elastic fibers in the alveolar walls stretch, and the air sacs of the lungs expand. During expiration, the external intercostals and diaphragm relax. In diseases such as asthma and COPD accessory muscles of respiration may be used: inspiration is assisted by the sternocleidomastoids and scalene muscles; expiration is aided by the internal intercostals and abdominal muscles.

Lung Volumes and Pulmonary Function Testing

Breathing in and out creates volumes that can be measured. In earlier times this was done with a spirometer, a revolving drum with a writing lever that recorded lung volumes on graph paper. Today a computer program is used.
The patient blows into a small hand-held device (flow sensor) and the results are displayed on a computer screen. Key elements are the forced vital capacity (FVC)—the maximum volume one can forcibly expel after a maximum inspiration (i.e., 4800 ml) and the forced expiratory volume in 1 second (FEV-1)—the amount of air forcibly expelled in 1 second (i.e., 83%).
The tidal volume (TV) is the amount of air moved during normal respiration. An asthmatic, for example, often has a normal TV and FVC but decreased FEV. In emphysema all three are usually decreased. The peak expiratory flow rate (PEFR), or peak flow, is a method of respiratory evaluation that can be done quickly in the emergency setting.
A small hand-held device (peak flow meter) is used. The maneuver is similar to the FVC but recorded in liters per minute (i.e., 550 L/min).
The Normal Respiratory Rate

The respiratory rate in adults is 12-18 breaths per minute. In the newborn it is about 40 and decreases to adult values at age 18. When a person realizes that the respiratory rate will be observed, he becomes self-conscious and begins to breathe in an odd fashion. Thus, the usual practice is to examine the heart or pulse and observe respirations without mentioning it.

The Physiology of Respiration

Oxygen from air enters the lungs and diffuses through the alveolar and capillary membranes into the bloodstream. The pulmonary veins return oxygen-rich blood to the left side of the heart, where it is pumped to the rest of the body via the aorta. Oxygen is transported in the blood as oxyhemoglobin in the red cells.
In the tissues, red cells move into the capillaries. At the arteriole end of the capillary, oxygen diffuses through the red cells, then through the capillary membrane into the tissue fluid. It then diffuses through the tissue cell membrane to be used as fuel for cellular metabolism.
Carbon dioxide moves out of tissue cells in the reverse direction into red cells, where most is converted to bicarbonate ion (HCO3-). Bicarbonate is transported in the plasma. The large veins bring oxygen-poor blood to the right side of the heart where it is transported via the pulmonary arteries to the lungs. In the lungs the process is reversed in the alveoli, and carbon dioxide is blown off.
Two tools are available for the analysis of the pH, oxygen and carbon dioxide content of blood. The pulse oximeter is a computer and probe consisting of 2 photodiodes and photodetector that attaches to the fingertip and measures the oxygen saturation of arterial blood. Blood gas analyzers, using blood gas and pH electrodes, measure the partial pressures of oxygen, carbon dioxide and pH of blood. Other values, such as oxygen saturation (Sa02) and bicarb level (HC03-) are calculated.

Regulation of Respiration

Respiration is controlled by the respiratory center, nerve cells in the reticular formation of the pons and medulla. Impulses from the cerebral cortex modify respirations, as do changes in the oxygen content, carbon dioxide content and the pH of blood. Cells sensitive to these changes are chemoreceptors, located in the medulla, the arch of the aorta (aortic bodies) and junction of the internal and external carotid arteries (carotid bodies).
Low oxygen, high carbon dioxide or low pH activates the chemoreceptors and causes the respiratory rate to increase. Low carbon dioxide or a high pH has the opposite effect. Impulses from the aortic and carotid bodies travel to the respiratory center in the brainstem via the vagus and glossopharyngeal nerves.

Acid/Base Conditions

The bicarbonate buffer equation illustrates the effects of various physiological conditions. Carbonic acid is transiently formed and carbon dioxide is blown off during expiration. In metabolic acidosis, a common problem, the body produces an increased amount of acid (H+), which combines with bicarbonate to form CO2 and water. In compensated metabolic acidosis, the body adjusts to keep the pH within normal limits. In uncompensated metabolic acidosis the body is unable to cope with the acid load and the pH begins to fall. The low pH stimulates the respiratory center and the equation shifts to the right. As H+ seen in diabetic ketoacidosis. An accumulation of acidic substances in kidney disease or aspirin overdose (impairment of oxidative phosphylation, a major buffer of H+) may also cause metabolic acidosis.
Treatment: The underlying cause is treated. If the pH is less than 7 or the HCO3- is becoming depleted, 1 or 2 amps of bicarbonate are given intravenously. In metabolic alkalosis, a rare condition, acid is lost, the equation shifts to the left to restore acid, and ventilation decreases. This is seen occasionally in those who have been vomiting for a long time (depletion of HCl from the stomach) and in those using diuretics (loss of H+ from the kidney).

Respiratory acidosis is seen in severe asthma, chronic obstructive pulmonary disease (COPD) and in conditions in which ventilation is poor, such as congestive heart failure and pneumonia. The person is unable to blow off CO2, which accumulates. The equation shifts to the left resulting in rising acidity. The respiratory rate increases in an effort to blow off accumulated CO2.
Treatment: increasing ventilation with bronchodilators. Occasionally intubation and assisted ventilation are required.

Respiratory alkalosis occurs as a compensatory reaction to metabolic acidosis and in anxiety reactions (hyperventilation syndrome—see next section). Treatment for hyperventilation is a quiet setting to restore CO2, and in the case of metabolic acidosis (i.e. ketoacidosis) the underlying condition is treated.
Often two acid-base conditions occur together. In diabetic ketoacidosis, as mentioned, the metabolic acidosis triggers a compensatory respiratory alkalosis. In this case, the HCO3 - is low, but so is the CO2. The pH will be close to normal. The person with COPD in respiratory acidosis may also have developed an additional metabolic acidosis. In this case, instead of the HCO3- being close to normal, it will fall. In general, if the pH is close to normal, and the CO2 and/or HCO3- are abnormal, one may assume a mixed condition.


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