Circulatory and Respiratory Physiology - Anatomy

Normal inspiration typically involves the flattening (contraction) of the diaphragm in order to increase the volume of the thoracic cavity, and can be done unconsciously. In order to increase the amount of inhaled air, other muscles such as the external intercostals and the sternocleidomastoids are included by conscious control. Both of these muscles aim to raise and expand the thoracic cavity in order to assist in inhalation.

The rectus abdominis is involved in the opposite action of forced exhalation. The rectus abdominis aims to decrease the volume of the thoracic cavity by contracting. This assists in forced exhalation.

Unconscious breathing is controlled by the pons and the medulla oblongata, both of which are parts of the brain stem. This unconscious breathing can be consciously controlled by using the cerebral cortex, which manages most voluntary actions.

It helps to remember that the brain stem is responsible for unconscious control of the body: breathing, heart rate, blood pressure, etc. It is the addition of the cerebral cortex that allows humans to have conscious control over actions, such as breathing, and override the unconscious controls. For example, the cerebral cortex is used to consciously stop breathing when diving underwater.

At rest the diaphragm is slightly curved superiorly such that it makes this sort of shape: When it contracts, it flattens out, with the middle of the muscle being pulled down until the muscle is roughly horizontal. Remembering that the diaphragm separates the thoracic and abdominal cavities, if it contracts, it physically increases the volume of the thoracic cavity. Now, remembering your fluid physics, an increase in volume is accompanied with a decrease in pressure. We know that high pressure flows to low pressure spontaneously. The atmospheric pressure is now higher than the intrapleural (or thoracic cavity) pressure, causing air to flow into the lungs.

Note that the external intercostals aid in inspiration and the internal intercostals aid in expiration.

Tidal volume is, by definition, the amount of air inspired/expired during normal breathing. The maximum volume of air that can be inspired after a normal expiration is the inspiratory capacity. The maximum volume of air that can be expired after a maximal inspiration is the vital capacity. The volume of air still in the lungs after a maximal expiration is the residual volume. The maximum volume of air that can be inspired after a normal inspiration is the inspiratory reserve volume.

During a respiratory cycle, the diaphragm contracts and moves downward. When this occurs the pressure in the alveoli falls. This pulls air into the lungs. At the same time external intercostals muscles contract, raising ribs and sternum and enlarges the cavity even more. During exhalation the diaphragm relaxes (moves up) and air is foced out of the body. A hiccup is a muscular spasm of the respiratory muscles including the diaphragm. A pneumothorax is a "hole" in the lungs that causes air to accumulate in the pleural space.

When exhaling, the lungs elasticity compresses the walls increasing the pressure within so that it exceeds atmospheric pressure and forces air out. Humans, despite how it might feel, do not suck in air. Rather pressure differences allow air to rush in and out. During expiration, the diaphragm relaxes, bowing up into the thoracic cavity, thereby decreasing the volume of the thoracic cavity. This results in a corresponding increase in pressure (Boyle's law), and thus the movement of air from the lungs out of the body through the upper respiratory structures.

The phrenic nerve is the nerve responsible for innervation of the diaphragm. The term phrenic is often associated with descriptions of the diaphragm (i.e cardiophrenic ligament is a ligament associated with connecting the diaphragm to the pericardium of the heart)

During the normal inspiratory phase of breathing, in other words, when a human is "breathing in," the physiological mechanism used is called "negative-pressure" breathing. Negative-pressure refers to the pressure in the chest cavity as compared to the surrounding environment. The body generates negative-pressure in the chest cavity during breathing by the contraction of the diaphragm muscle (it pulls downward, expanding the thoracic cavity size and space for the lungs to fill), and the outward expansion of the ribcage (which also expands the thoracic cavity size and provides more space for the lungs to fill). With the increased volume of the thoracic cavity generated, this creates the negative pressure that is needed to draw air into the lungs down its gradient of higher pressure (outside the body/thorax) to lower pressure (into the lungs/thorax). Positive-pressure is an incorrect choice because it is the opposite of what occurs during normal human inspiration.

Positive-pressure is sometimes artificially used in the medical setting with machines in patients with obstructive sleep apnea, or in patients who cannot breathe on their own, but is not a part of standard physiological respiration. The Frank-Starling mechanism describes the mechanism by which the heart pumps blood, but does not describe respiration. Glomerular filtration describes the mechanism by which the glomeruli of the kidneys initially filter blood, but does not describe respiration. Idiopathic pulmonary fibrosis is a disease of the interstitium of lung tissue, but does not describe the physiological mechanism used during inspiration.

In this patient with Chronic Obstructive Pulmonary Disease (COPD), which is a disease that results in difficulty expiring air (and generally does not affect one's ability to inspire air), we would expect to see an increased level of in the air that he/she expires, as compared to someone without COPD. Although this is a medically-oriented question, this does not require you to know anything about COPD that is not already supplied in the question. By stating that the ability to expire air is impacted but that the ability to inspire is generally not affected, this calls upon your knowledge of pulmonary physiology, telling you that if inspiration is not affected, levels are probably not significantly affected, and that if expiration is affected, levels are probably affected.

Once you identify that levels are affected in COPD, the question now is, how exactly are they affected? In a COPD patient, it is stated in the question stem, that they have a decreased ability to expire air. When a healthy person expires air, they remove from the body. In a COPD patient, who therefore has a decreased ability to remove from the lungs, if we measured the amount of a in a single breath, we would expect it to be elevated as compared to a healthy individual. At first glance, this may seem counter-intuitive, since we are stating that COPD patients have trouble removing from the body. However, the air that they expire is the same air that is coming from their lungs, which contains the elevated levels of . Thus, to answer the question, we expect the reading for the expired breath to be elevated as compared to that of a healthy person.

During forced maximum expiration, the lungs are trying their best to push air out of the lungs with the most force. This cannot be accomplished by the lungs alone, so the additional contraction of the abdominal muscles aid to help push air out of the lungs with maximum force.

This is different from normal (quiet) expiration, where only the elastic recoil of the lungs are needed with no additional muscle contractions. Normal expiration does not require pushing air out of the lungs with force.

None of the volumes listed would be normal. The internal intercostal muscles contribute to forced expiration and would affect ERV, TLC and VC. The external intercostal muscles contribute to inspiration and would affect the IRV, TLC and VC. Thus, none of the above volumes could be normal in a man who has non-functioning intercostal muscles.

When exercising, the muscles of inspiration include: external intercostals, scalene muscles, sternocleidomastoids.

When exercising, the muscles of expiration include: rectus abdominis, internal and external obliques, transversus abdominis, internal intercostals.

The main inspiratory muscle involved in quiet breathing is the diaphragm, which is a dome shaped sheet of skeletal muscle that is attached to the ribs, sternum, and vertebral column. External intercostals are also involved in quiet breathing, but if these muscles were impaired, quiet breathing would still continue because the diaphragm is the main muscle involved. Accessory muscles are not involved in quiet breathing, but may become involved during exercise. The abdominal wall muscles and internal muscles are both involved in expiration.

Epinephrine is a hormone secreted in order to facilitate "fight or flight" reactions by the body. Secretion of epinephrine from the adrenal medulla is initiated by sympathetic stimulation. Epinephrine will increase heart rate, blood pressure, and contraction force; however, the skeletal muscle arterioles will be dilated so that more blood is able to reach the muscles. The sympathetic nervous system is designed to direct blood toward skeletal muscle and the heart, and away from the digestive tract and skin.

A lipid soluble hormone is likely to make its way to the nucleus because it can easily pass through the hydrophobic membranes of cells. A water soluble protein is likely to attach to the outside of a cell and activate a signaling pathway since it cannot readily pass through the phospholipid bilayer (cell membrane). Hydrophilic hormones are the same as water soluble hormones. Fat soluble hormones must be carried by proteins through the blood.

Hormones secreted into the blood stream have the ability to travel anywhere in the body. Such hormones are endocrine hormones and they can act on organs far from their source. Substances that are secreted outside the body (or within a body cavity) are not hormones, since all hormones are released by endocrine glands into the blood. Rather, these substances are released by exocrine glands (i.e. sweat, digestive enzymes).

Norepinephrine and epinephrine (on about an equal basis) on beta-1 receptors in the heart increase heart rate and contractility (force of contraction). These hormones are released from the adrenals in response to sympathetic stimulation.

Moving the heart rate between 60 and 100 bpm involves only the addition and removal of parasympathetic tone. Remember, parasympathetic: rest and digest; so, to raise the heart rate, parasympathetic tone would have to be withdrawn. Sympathetic tone would not be added until the heart rate exceeds 100 bpm.

Veins always carry blood towards the heart. The blood in veins is mostly deoxygenated, however the pulmonary vein, which goes from the lungs to the left atrium, carries newly oxygenated blood back to the heart for it to be pumped to the rest of the body.

In contrast, arteries always travel away from the heart and usually carry oxygenated blood, with the exception of the pulmonary arteries. Arteries and arterioles have a thick layer of smooth muscle that helps to regulate blood pressure. Veins may have some smooth muscle, but are not nearly as significant in helping to regulate blood flow.

A common misconception is that all veins carry deoxygenated blood. In reality, all veins are responsible for bringing blood back to the heart. Generally, blood traveling toward the heart is deoxygentated. The pulmonary veins, however, bring blood that has just received oxygen from the lungs back to the heart. The pulmonary veins are the only veins in the body to carry oxygenated blood.

Similarly, the pulmonary arteries are the only arteries to carry deoxygentated blood away from the heart. All arteries carry blood away from the heart, but most contain oxygenated blood. The vena cavae are large veins that carry deoxygenated blood from the body back to the right atrium. This blood is then transferred to the right ventricle, and the then pulmonary arteries for transport to the lungs. The path of blood from the heart to the lungs and back is known as the pulmonary circuit.