The individual's blood pH level will decrease (become more acidic). The increase in CO₂ will cause the carbonic anhydrase reaction to shift to the right, increasing the concentration of protons (H⁺) in the blood. The individual can raise their pH level back to normal by breathing out all of the excess CO₂. This accounts, in part, for increased respiration rates during exercise (along with the increased demand for oxygen).

Slightly increased levels, or partial pressures, of carbon dioxide (CO₂) would signal for an increase in breathing rate. As CO₂ levels in the blood rise due to the breathing of such air as described in the passage, a breathing mechanism in the brain is triggered to increase ventilation (hyperventilation) to remove as much CO₂ through the lungs as possible. A decrease in breathing rate would build up CO₂ to even higher levels, causing respiratory acidosis. There would be no changes to blood pressure because slight increases of CO₂ has no significant effect on this property.

It is important to know that the medulla oblongata in the brainstem is the site of breathing rate control. pH receptors at the medulla sense the hydrogen concentration in the blood, and increase or decrease the rate of breathing to alter bicarbonate levels in the blood, maintaining healthy pH levels.

The cerebellum is involved in balance and coordination, while the frontal cortex and occipital lobe are both regions of the cerebrum, involved in higher thinking, processing, and voluntary actions.

The total lung capacity is the maximum amount of air that can fill the lungs.

The vital capacity is the amount of air that can be exhaled after fully inhaling.

The tidal volume is the amount of air inhaled during normal, relaxed breathing.

The expiratory reserve volume is the amount of air that can be forcibly exhaled after a normal exhalation.

The inspiratory reserve volume is the amount of air that can be forcibly inhaled after a normal inhalation.

The residual volume is the amount of air still remaining in the lungs after the expiratory reserve volume is exhaled.

By adding the residual volume and vital capacity, you can obtain a value for the total lung capacity.

Epinephrine binds to the beta-2 receptor. The binding of epinephrine to the beta-2 receptor causes bronchodilation by relaxing the smooth muscles surrounding the airway. The relaxation of the smooth muscles around the airway increases the airway diameter and therefore allows the patient to breathe easier.  

Oxygenated blood returning to the heart from the lungs enters the left atrium. It then goes to the left ventricle and out the aorta.

The correct electrical path through the heart is the SA (sinoatrial) node, AV (atrioventricular) node, bundle of His (AV bundle), then purkinje fibers.

The sinoatrial node initiates the electrical signal and acts as the heart's natural pacemaker. Innervation from the parasympathetic nervous system is crucial in maintaining a normal heart rate from the SA node, but is not required to initiate electrical signals. The signal travels to the atrioventricular node and is briefly delayed, allowing the atria to finish contracting before initiaing ventricular systole. The signal travels down the bundle of His and is quickly distributed to the purkinje fibers, which initiate ventricular systole.

The tricuspid valve separates the right atrium from the right ventricle. The bicuspid valve (also known as the mitral valve) separates the left atrium from the left ventricle. The pulmonic valve separates the right ventricle from the pulmonary artery and the aortic valve separates the left ventricle from the aorta (these are known as the semilunar valves).

Cardiac output is the product of heart rate (HR) and stroke volume (SV). Heart rate is equal to beats per minute, while stroke volume is equal to volume per beat. The "beat" units cancel, and leave the cardiac output equal to volume per minute.

cardiac output = (beats/min) * (volume/beat) = volume/min. 

Electrical coupling of cells is mediated through gap junctions—ions are able to immediately flow through adjacent cells through these transmembrane protein channels. Cardiac muscle requires such syncytial connections in order to most effectivey synchronize muscle contraction.

Neurotransmitters, synaptic junctions, and cholinergic receptors would necessitate a nervous system communication, but the heart is electrically-coupled without neural mediation. Pressure receptors are not involved in cardiac muscle activity.