



Respiratory System Under Stress

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Respiratory System Under Stress


L.Ebihara MD-PhD

Assigned reading: Chapt. 9. from West


In this lecture we will examine the responses of the respiratory system to three physiological stresses as they relate to material covered in previous lectures. The three stresses that will be discussed in lecture are: exercise, ascent to altitude, and diving. You should also read and be familiar with the material in Chapter 9 in West. The student should be able to:


  1. Identify the physiological stresses involved in exercise.
  2. Predict the responses of the respiratory system to acute exercise.
  3. Describe the effects of long-term exercise programs on the respiratory system.
  4. Identify the physiological stresses involved in ascent to high altitudes.
  5. Predict the initial responses of the respiratory system to high altitude.
  6. Describe the acclimatization of the cardiovascular and respiratory systems to residence at high altitudes.
  7. Identify the physiological stresses in diving
  8. Predict the responses of the respiratory system to various types of diving


I. Exercise


  • Stresses the respiratory system by increasing the demand for oxygen and increasing the production of carbon dioxide. Moderate to severe exercise also increase lactic acid production
  • Response to stress: The respiratory and cardiovascular system must increase the volume of oxygen supplied to exercising tissues and increase the removal of carbon dioxide and hydrogen ions from the body.
  • Acute Effects
    • Metabolic changes-↑Oxygen consumption (VO2), ↑carbon dioxide production (VCO2)
    • Cardiac changes- VO2 is related to cardiac output by the Fick equation:

VO2 = CO x (CaO2-CvO2)

where CO is the cardiac output in ml/min, and (CaO2-CvO2) is the arterial-venous oxygen content difference in ml/100 ml blood. Since cardiac output is the product of stroke volume (SV) and heart rate (HR),

VO2 = SV x HR x (CaO2-CvO2)

Both SV and HR increase immediately with exercise, but stroke volume plateaus early. Further increases in cardiac output are largely due to increases in heart rate.

    • Systemic circulation changes: The increase in CO causes more blood to

be delivered to exercising muscles. In addition, there is a redistribution of the systemic circulation involving vasodilation in the skin and working muscles.

    • Oxygen extraction changes: Apart from increased cardiac output and

vascular redistribution, a third mechanism to meet oxygen requirements is increased oxygen extraction from arterial blood; this results in an increased arterial-venous oxygen content difference.

    • Pulmonary circulation changes. The pulmonary circulation increases. Mean pulmonary artery pressure rises only slightly despite the large increase in CO. This indicates a decrease in pulmonary vascular resistance (PVR) due to the distention and recruitment of pulmonary capillaries. There is also a redistribution of blood flow so that the blood flows more uniformly to all parts of the lung.
    • Ventilation changes. As pulmonary blood flow increases, both minute

ventilation (VE) and alveolar ventilation (VA) increase; in this way the lungs transfer more oxygen and carbon dioxide. Although both tidal volume (VT) and respiratory rate increase with exercise, in the early stages an increase in VT accounts for most of the rise in VE and VA.

  • Effects of graded exercise
    • Metabolism during exercise. There are two types of exercise: aerobic and anaerobic. Mild exercise is primarily aerobic. During moderate to severe levels of exercise, anaerobic metabolism occurs in addition to ongoing aerobic metabolism. The point at which anaerobic metabolism begins is called the threshold for anaerobic metabolism (AT). Above AT, lactic acid builds up.
    • Respiratory quotient (RQ), measured as carbon dioxide elimination over oxygen uptake by the lungs, increases as work increases. During mild to moderate exercise RQ is about 0.85. At AT, RQ goes above 1 due to H+ buffered by HCO2-.
    • As work increases, VCO2, VA, and VE increase proportionally so that PaCO2 remains constant until the anaerobic metabolism begins (see figure 1). After AT is reached, VE and VA rise more steeply than VCO2, so PaCO2 falls; this hyperventilation occurs as compensation for the lactic acidosis.

Figure 1. Effect of graded exercise on different parameters. Note that both PaO2 and PaCO2 remain constant during moderate exercise.

    • As work increases, VO2 increases in a linear fashion and eventually plateaus as shown in Figure 2. This plateau, which for a healthy person occurs only after the onset of anaerobic threshold (very heavy exercise), is called VO2max. The work rate can increase beyond VO2max, but the rate of oxygen uptake will remain flat because the cardiac output cannot increase further. For most adults without cardiopulmonary disease, VO2max is reached between 2 and 3 L/minute, which is approximately 10 times the resting VO2. World class athletes can reach a VO2max of over 4 L/minute.

Figure 2

    • It is important to note that in a normal person the resting minute ventilation can be increased ~20X whereas maximal increases in the cardiac output during exercise are only about 4-6X. Therefore, it is the cardiovascular system rather than the respiratory system that is the limiting factor in exercise in a normal person.
    • Explaining the ventilatory response to exercise shows that the simple reflex viewpoint of ventilatory control is woefully inadequate. During mild and moderate exercise, the PaCO2 does not change even though ventilation has increased many fold. This implies a remarkable coupling between ventilation and carbon dioxide production that is not dependent on an “error signal” from the chemoreceptors. At high work loads, a lactic acidosis develops and this additional stimulus causes PaCO2 to decrease below normal levels. Explaining the response to exercise has been one of the main problems in respiratory physiology throughout the 20th century and is still a challenge in the 21st century.
  • Effects on long term training programs
    • The main effect is an increase in the maximal cardiac output due to increased stroke volume. The maximal heart rate is not affected by training but the heart rate of a trained athlete is lower than that of an untrained person at any level of physical activity.
    • Increases oxidative capacity of skeletal muscle.


II. Ascent to high altitudes


As one ascends to greater heights, the total barometric pressure decreases because the barometric pressure at any altitude is proportional to the weight of the air above it. The change in barometric pressure per change in vertical distance is not constant as shown in Figure 9-2 from West.

The alveolar PO2 (PAO2) can be calculated using the alveolar gas equation:

The fractional concentration of oxygen in the atmosphere does not change with altitude. It is always about .21.


Water vapor pressure depends on the temperature and humidity of air. However, inspired air is always warmed to body temperature and completely humidified so that the partial pressure of water vapor in inspired air is always 47 mm Hg.


Therefore PIO2 is equal to

  • Acute Effects
    • Hypoxia stimulates arterial chemoreceptors which stimulate the rate and depth of breathing. This causes a decrease in alveolar and arterial PCO2, thereby allowing alveolar PO2 to increase.
    • As PACO2 falls, the pH of blood increases.
    • Heart rate and blood pressure initially increase.
  • Acclimatization - defined as the process of physiological change in the body that increases oxygen delivery to the tissues over a period of hours to days or weeks. The most important changes are listed below.
    • Ventilation and pH changes - First, hyperventilation occurs in response to hypoxemia. This results in alkalosis and elevated CSF pH which tends to limit the ventilatory response. The kidneys respond by increasing bicarbonate excretion in order to return the blood and CSF pH to near their normal values. This response starts within 24 hours and lasts for several days. The return of CSF pH toward normal results in more stimulation of central chemoreceptors and causes ventilation to increase further. Yet, measurement of CSF pH has not fully supported this theory. An alternate hypothesis is that the carotid bodies adapt and increase their sensitivity to hypoxia over several days and thus provide more ventilatory stimulation. In animals, chronic exposure to hypoxia causes carotid body hypertrophy with an increase in dopamine content as well as in other neurotransmitters. Physiological studies in both animals and humans indicate that the carotid body sensitivity does increase with prolonged hypoxia and this is now thought to be the primary mechanism for altitude adaptation.
    • Heart rate and blood pressure slowly return toward low altitude values.
    • On a time scale of days to weeks, the concentration of oxygen-carrying red blood cells increase (polycythemia) due to increased production of new red blood cells.


III. Diving


  • Diving physics
    • During diving, the pressure increases by 1 atmosphere for every 33 ft of descent.
    • Boyle’s law - This law of physics determines the volume of gases and accounts for the major portion of diving medical problems. Stated simply, the volume of gases are reduced when pressure is increased (diver descending) and the volume is increased on reduction of pressure (diver ascending).
    • Henry’s law - This rule explains the evolution of bubbles in a solution. It states that the volume of a gas is directly proportional to the pressure above a liquid.
  • Breath-hold diving – At the moment a diver holds his breath, the mass of air in the lungs is fixed; no new air can enter or leave. Under these conditions, Boyle’s law predicts that the lungs will shrink on descent and re-expand on ascent.
  • Scuba diving – The situation is different for scuba diving because compressed air is being continuously inhaled. The fresh air is at the same pressure as the surrounding water pressure. As long as the diver continously breathes from the scuba tank, the density of inhaled air will change with ascent and descent. However, if the scuba diver holds his breath and attempts to ascend, the fixed mass of gas at the time of breath-hold would expand in volume (as predicted by Boyle’s law) until the diver exhaled or the lungs ruptured (see figure below). This is why breath holding during ascent is so dangerous.The most serious complication of a ruptured lung is an air embolism which is when escaped air enters the pulmonary veins, from where it can travel to the arterial circulation.

  • Decompression sickness – Nitrogen is poorly soluble at normal atmospheric pressure. However, Henry's and Dalton's Laws predict that, as the diver descends, excess nitrogen will enter the blood and all body tissues. These laws also predict that, on ascent (as ambient pressure decreases) the extra nitrogen that accumulated will diffuse out of the tissues and into the circulation. DCS arises when excess dissolved nitrogen forms bubbles large enough to cause symptoms during rapid ascent. The only treatment for DCS is recompression in a hyperbaric chamber
  • Nitrogen narcosis – As the partial pressure of nitrogen increases, various CNS effects occur, such as: euphoria, loss of coordination, and eventually coma.
  • Oxygen toxicity - Since the pressure of all inhaled gases increases with increasing depth, there is risk of inhaling too much oxygen and developing oxygen toxicity. However, this is unlikely to occur in recreational diving because the recreational diver is exposed to high oxygen pressures, but not long enough to risk oxygen toxicity. The problem is a potential hazard at greater depths, or when breathing mixtures containing more than 21% oxygen (e.g., nitrox).

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