question: What causes the pressure in our chest when we hold our breath?
comment: The pressure doesn't actually increase as you hold your breath. What you are feeling is the psychological manifestation of your need to breathe. And what is ultimately driving that is increased carbonic acid in your blood. Carbon dioxide is a bit different from other gases in that it doesn't really dissolve in water, but rather almost completely breaks down and reforms into carbonic acid. That acidity of this causes the pH of your blood to lower while you hold your breath, and it is that change in pH that drives you to take another breath long before you actually need to to get more oxygen.
passages: The partial pressure of gas in blood is significant because it is directly related to ventilation and oxygenation. When used alongside the pH balance of the blood, the PCO and HCO (and Lactate) suggest to the health care practitioner which interventions, if any, should be made.
  
  Section::::Equations.
  
  Section::::Equations.:Oxygen content.
   The partial pressure of oxygen and carbon dioxide in the arterial blood is monitored by the peripheral chemoreceptors (PNS) in the carotid artery and aortic arch. A change in the partial pressure of carbon dioxide is detected as altered pH in the cerebrospinal fluid by central chemoreceptors (CNS) in the medulla oblongata of the brainstem. Information from these sets of sensors is sent to the respiratory center which activates the effector organs – the diaphragm and other muscles of respiration. An increased level of carbon dioxide in the blood, or a decreased level of oxygen, will result in a deeper breathing pattern and increased respiratory rate to bring the blood gases back to equilibrium.
   Ventricular pressure is a measure of blood pressure within the ventricles of the heart.
  
  Section::::Function.:Pressures.:Left.
  
  During most of the cardiac cycle, ventricular pressure is less than the pressure in the aorta, but during systole, the ventricular pressure rapidly increases, and the two pressures become equal to each other (represented by the junction of the blue and red lines on the diagram on this page), the aortic valve opens, and blood is pumped to the body.
  
  Elevated left ventricular end-diastolic pressure has been described as a risk factor in cardiac surgery.
  
  Noninvasive approximations have been described.
   Lung volume decreases in the upright position due to cranial displacement of the abdomen due to hydrostatic pressure, and resistance to air flow in the airways increases significantly because of the decrease in lung volume.
  
  Hydrostatic pressure differences between the interior of the lung and the breathing gas delivery, increased breathing gas density due to ambient pressure, and increased flow resistance due to higher breathing rates may all cause increased work of breathing and fatigue of the respiratory muscles.
   All the blood returning from the body tissues to the right side of the heart flows through the alveolar capillaries before being pumped around the body again. On its passage through the lungs the blood comes into close contact with the alveolar air, separated from it by a very thin diffusion membrane which is only, on average, about 2 μm thick. The gas pressures in the blood will therefore rapidly equilibrate with those in the alveoli, ensuring that the arterial blood that circulates to all the tissues throughout the body has an oxygen tension of 13−14 kPa (100 mmHg), and a carbon dioxide tension of 5.3 kPa (40 mmHg). These arterial partial pressures of oxygen and carbon dioxide are homeostatically controlled. A rise in the arterial formula_3, and, to a lesser extent, a fall in the arterial formula_3, will reflexly cause deeper and faster breathing till the blood gas tensions return to normal. The converse happens when the carbon dioxide tension falls, or, again to a lesser extent, the oxygen tension rises: the rate and depth of breathing are reduced till blood gas normality is restored.
   Similarly, baroreceptors are stretch receptors located in the aortic sinus, carotid bodies, the venae cavae, and other locations, including pulmonary vessels and the right side of the heart itself. Rates of firing from the baroreceptors represent blood pressure, level of physical activity, and the relative distribution of blood. The cardiac centers monitor baroreceptor firing to maintain cardiac homeostasis, a mechanism called the baroreceptor reflex. With increased pressure and stretch, the rate of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase parasympathetic stimulation. As pressure and stretch decrease, the rate of baroreceptor firing decreases, and the cardiac centers increase sympathetic stimulation and decrease parasympathetic stimulation.
   At the beginning of the cardiac cycle, the ventricles are relaxing. As they do so, they are filled by blood passing through the open mitral and tricuspid valves. After the ventricles have completed most of their filling, the atria contract, forcing further blood into the ventricles and priming the pump. Next, the ventricles start to contract. As the pressure rises within the cavities of the ventricles, the mitral and tricuspid valves are forced shut. As the pressure within the ventricles rises further, exceeding the pressure with the aorta and pulmonary arteries, the aortic and pulmonary valves open. Blood is ejected from the heart, causing the pressure within the ventricles to fall. Simultaneously, the atria refill as blood flows into the right atrium through the superior and inferior vena cavae, and into the left atrium through the pulmonary veins. Finally, when the pressure within the ventricles falls below the pressure within the aorta and pulmonary arteries, the aortic and pulmonary valves close. The ventricles start to relax, the mitral and tricuspid valves open, and the cycle begins again. 
   Increased blood pressure in the capillaries of the lung causes pulmonary hypertension, leading to interstitial edema if the pressure increases to above 20 mmHg, and to pulmonary edema at pressures above 25 mmHg.
  
  Section::::Mean systemic pressure.
  
  If the heart is stopped, blood pressure falls, but it does not fall to zero. The remaining pressure measured after cessation of the heart beat and redistribution of blood throughout the circulation is termed the mean systemic pressure or mean circulatory filling pressure; typically this is of the order of ~7mm Hg.
  
  Section::::Disorders of blood pressure.
   During exhalation, the diaphragm relaxes, moving upward, and decreases the size of the chest cavity, causing an increase in intrathoracic pressure. This increase in pressure inhibits venous return to the heart resulting in both reduced atrial expansion and reduced activation of baroreceptors. This relieves the suppression of vagal tone and leads to a decreased heart rate.
  
  Section::::Noninvasive vagal tone quantification.:Respiratory sinus arrhythmia.:RSA as a vagal tone estimator.
   Section::::Venous return.
  
  As venous return increases, the pressure in the superior and inferior vena cava increase. This results in an increase in the pressure of the right atrium, which stimulates the atrial stretch receptors (low pressure receptor zones). These receptors in turn signal the medullary control centers to increase the heart rate (Tachycardia). Unusually, this tachycardia is mediated by increased sympathetic activity to the sinoatrial node (SAN) with no fall in parasympathetic activity.
   The resulting arterial partial pressures of oxygen and carbon dioxide are homeostatically controlled. A rise in the arterial partial pressure of CO and, to a lesser extent, a fall in the arterial partial pressure of O, will reflexly cause deeper and faster breathing till the blood gas tensions in the lungs, and therefore the arterial blood, return to normal. The converse happens when the carbon dioxide tension falls, or, again to a lesser extent, the oxygen tension rises: the rate and depth of breathing are reduced till blood gas normality is restored.
   Alveolar pressure (PA) at end expiration is equal to atmospheric pressure (0 cm H20 differential pressure, at zero flow), plus or minus 2 cm H2O (1.5 mmHg) throughout the lung. On the other hand, gravity causes a gradient in blood pressure between the top and bottom of the lung of 20 mmHg in the erect position (roughly half of that in the supine position). Overall, mean pulmonary venous pressure is ~5 mmHg. Local venous pressure falls to -5 at the apexes and rises to +15 mmHg at the bases, again for the erect lung.
   Atrial bradycardias are divided into three types. The first, respiratory sinus arrhythmia, is usually found in young and healthy adults. Heart rate increases during inhalation and decreases during exhalation. This is thought to be caused by changes in the vagal tone during respiration. If the decrease during exhalation drops the heart rate below 60 bpm on each breath, this type of bradycardia is usually deemed benign and a sign of good autonomic tone.
   Alveolar pressure
  
  Alveolar pressure (P) is the pressure of air inside the lung alveoli. When the glottis is opened and no air is flowing into or out of the lungs, alveolar pressure is equal (zero cmH2O).
  
  Section::::Significance.
  
  During inspiration, the increased volume of alveoli as a result of lung expansion decrease the intra-alveolar pressure to a value below atmospheric pressure about -1 cmH2O. This slight negative pressure is enough to move 500 ml of air into the lungs in 2 seconds required for inspiration. At the end of inspiration, the alveolar pressure returns to atmospheric pressure (zero cmH2O).
   The most important function of breathing is the supplying of oxygen to the body and the removal of its waste product of carbon dioxide. Under most conditions, the partial pressure of carbon dioxide (PCO2), or concentration of carbon dioxide, controls the respiratory rate.
   There appears to be a connection between pulmonary edema and increased pulmonary blood flow and pressure which results in capillary engorgement. This may occur during higher intensity exercise while immersed or submersed.
  
  Facial immersion at the time of initiating breath-hold is a necessary factor for maximising the mammalian diving reflex in humans.
  
  Section::::Physiological response.:Thermal balance responses.
   Similarly, baroreceptors are stretch receptors located in the aortic sinus, carotid bodies, the venae cavae, and other locations, including pulmonary vessels and the right side of the heart itself. Rates of firing from the baroreceptors represent blood pressure, level of physical activity, and the relative distribution of blood. The cardiac centers monitor baroreceptor firing to maintain cardiac homeostasis, a mechanism called the baroreceptor reflex. With increased pressure and stretch, the rate of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase parasympathetic stimulation. As pressure and stretch decrease, the rate of baroreceptor firing decreases, and the cardiac centers increase sympathetic stimulation and decrease parasympathetic stimulation.
   BULLET::::- Central venous pressure, which is a good approximation of right atrial pressure, which is a major determinant of right ventricular end diastolic volume. (However, there can be exceptions in some cases.)
  
  BULLET::::- The jugular venous pressure (JVP) is the indirectly observed pressure over the venous system. It can be useful in the differentiation of different forms of heart and lung disease.
  
  BULLET::::- The portal venous pressure is the blood pressure in the portal vein. It is normally 5–10 mmHg
  
  Section::::Pulmonary pressure.
  
  Normally, the pressure in the pulmonary artery is about 15 mmHg at rest.
   Section::::Rate and depth of breathing.
  
  Early physiologists believed the reflex plays a major role in establishing the rate and depth of breathing in humans. While this may be true for most animals, it is not the case for most adult humans at rest. However, the reflex may determine breathing rate and depth in newborns and in adult humans when tidal volume is more than 1 L, as when exercising.
  
  Section::::Hering–Breuer deflation reflex.
   By early maturity, the walls of the left ventricle have thickened from three to six times greater than that of the right ventricle. This reflects the typical five times greater pressure workload this chamber performs while accepting blood returning from the pulmonary veins at ~80mmHg pressure (equivalent to around 11 kPa) and pushing it forward to the typical ~120mmHg pressure (around 16.3 kPa) in the aorta during each heartbeat. (The pressures stated are resting values and stated as relative to surrounding atmospheric which is the typical "0" reference pressure used in medicine.)
  
  Section::::Function.
   Bainbridge Reflex is involved in Respiratory Sinus Arrhythmia. During inhalation intrathoracic pressure decreases. It triggers increased venous return which is registered by stretch receptors, which via Bainbridge Reflex increases the heart rate momentarily during inspiration. This is not to be confused with stage 4 of the Valsalva maneuver, in which the release of high intrathoracic pressure previously generated by forced expiration against a closed glottis, now restores venous return and cardiac output into a vasoconstricted circulation, stimulating the vagus nerve and leading to a slowing of the heart, or bradycardia.
  
  Section::::See also.
  
  BULLET::::- Low pressure receptor zones
   An elevated pressure difference between the aortic pressure and the left ventricular pressure may be indicative of aortic stenosis.
  
  Section::::Function.:Pressures.:Right.
  
  Right ventricular pressure demonstrates a different pressure-volume loop than left ventricular pressure.
  
  Section::::Function.:Dimensions.
   Section::::PV loop changes for diverse cardiac abnormalities.:Restrictive cardiomyopathy.
  
  Restrictive cardiomyopathy includes a group of heart disorders in which the walls of the ventricles become stiff (but not necessarily thickened) and resist normal filling with blood between heartbeats.
  
  This condition occurs when heart muscle is gradually infiltrated or replaced by scar tissue or when abnormal substances accumulate in the heart muscle. The ventricular systolic pressure remains normal, diastolic pressure is elevated and the cardiac output is reduced.
  
  Section::::PV loop changes for diverse cardiac abnormalities.:Valve diseases.
  
  Section::::PV loop changes for diverse cardiac abnormalities.:Valve diseases.:Aortic stenosis.
   Pressure support ventilation
  
  Pressure support ventilation (PSV), also known as pressure support, is a spontaneous mode of ventilation. The patient initiates every breath and the ventilator delivers support with the preset pressure value. With support from the ventilator, the patient also regulates his own respiratory rate and tidal volume.
   Increasing the heart rate serves to decrease the pressure in the superior and inferior venae cavae by drawing more blood out of the right atrium. This results in a decrease in atrial pressure, which serves to bring in more blood from the vena cavae, resulting in a decrease in the venous pressure of the great veins. This continues until right atrial blood pressure returns to normal levels, upon which the heart rate decreases to its original level.
  
  Section::::Respiratory Sinus Arrhythmia.
  
presuppositions: Pressure in our chest increases when we hold our breath. Holding your breath causes an increase in pressure on your chest.
corrections: Pressure in our chest does not increase when we hold our breath. There is no increased pressure in the chest, there is an increase of carbonic acid in the blood which develops a need to breathe.
raw_presuppositions: Pressure in our chest increases when we hold our breath. Holding your breath causes an increase in pressure on your chest.
raw_corrections: Pressure in our chest does not increase when we hold our breath. There is no increased pressure in the chest, there is an increase of carbonic acid in the blood which develops a need to breathe.