Respiratory: The Physiology of Altitude, Exercise, and Diving

Minor diving injuries are called ______ because ______.

"squeeze injuries;" damage to soft tissues are caused by increased pressure

Symptoms of High Altitude Pulmonary Edema

1. Dyspnea with Minimal Exertion 2. Slow Recovery from Exercise 3. Tachycardia at Rest 4. Tachypnea at Rest 5. Dry Cough: This can progress to a frothy pink sputum. 6. Bilateral or Unilateral Inhomogeneous Alveolar Infiltrates Symptoms are most commonly noted on the second night at increased altitudes.

Symptoms of acute mountain sickness include: (5)

1. Headache 2. Fatigue 3. Sleep Disturbances 4. Dizziness 5. Anorexia * Symptoms may develop 4 to 36 hours after arrival and usually abate spontaneously over a few days with no further ascent and/or sleeping at lower altitudes.

How is high altitude pulmonary edema prevented? (4)

1. High altitude pulmonary edema can be prevented with a gradual descent and recognition of early AMS symptoms so that the ascent is stopped before HAPE develops. 2. With a previous history of high altitude pulmonary edema, nifedipine 20 mg slow release every 8 hours (of tadalafil 10 mg every eight hours starting with the ascent or dexamethasone 8 mg every 12 hours starting two days prior to ascent) can be taken during the accent, and then continued for three days following the descent. However, the patient must be monitored for hypotension. 3. An inhaled β-adrenergic agonist can be used. 4. Acetazolamide can be effective as well.

How are diving injuries treated? (3)

1. Hyperbaric therapy is the mainstay of treatment and should be instituted with recompression as soon as possible along with the administration of oxygen. Once stabilized, patient must be decompressed to permit inert gases to be carried away from tissues and back to lungs to be exhaled (off-gassing). 2. Patients often receive fluid replacement, as they are often dehydrated. 3. Patients receive antiplatelet therapy, as there is often damage to the microvascular endothelium from inert free gas. * With early treatment, recovery is excellent. However, with delayed therapy, diving injuries can lead to permanent brain and spinal cord damage.

pIO2 =

0.21 (PB - PH2O) PB: Barometric Pressure PH2O: Partial Pressure of H2O

What are three clinical problems with altitude?

1. Acute Mountain Sickness 2. High Altitude Cerebral Edema (HACE) 3. High Altitude Pulmonary Edema (HAPE)

How is decompression sickness prevented? (2)

1. Decompression sickness can be prevented by controlling the rate and duration of compression and decompression. 2. Decompression sickness can be prevented through an altered gas mix (i.e. low FiO2 to prevent oxygen toxicity, low FiN2 to prevent nitrogen narcosis and prevent increased PaN2, and adding helium which is not very soluble in water, decreases work of breathing, and is non- "narcotic").

What are the three phases of the ventilatory response to exercise within the first minute?

1. During the first minute of exercise, there is an immediate increase in alveolar ventilation as we exercise due to neuronal stimulation. The higher centers of the brain can send signals to the respiratory centers to increase ventilation for exercise. Furthermore, receptors of the joints and muscles also send signals to the respiratory center that movement is occurring in order to stimulate ventilation. This causes a decrease in the alveolar and arterial pCO2 because, at this early stage, not much CO2 has been produced. 2. This increase in ventilation causes a decrease in the alveolar and arterial pCO2 because, at this early stage, not much CO2 has been produced. CO2 will diffuse into the CSF and interstitial fluid around the medulla. CO2 reacts with water to produce H2CO3, which dissociates into HCO3- and H+. These H+ ions then stimulate the chemosensitive area. Because there is a drop in the arterial and alveolar pCO2 and a drop in the H+ that stimulate the chemosensitive area, there is an initial drop in the ventilatory response. However, as exercise continues, producing more CO2 and utilizing more O2, then alveolar ventilation increases because the pCO2 increases. 3. However, as long as exercise is not too strenuous, then a steady-state level of alveolar ventilation is reached.

What is the effect of altitude on alveolar ventilation?

Regarding alveolar ventilation, altitude results in more uniform ventilation because of deeper inspirations and expirations.

What are the two major effects of high altitude on cerebral blood flow?

1. Hypoxia can lead to hyperperfusion, which leads to the distension of cerebral vessels. As a result, fluid leakage, edema, and increased intracranial pressure may result. 2. With an increased ventilation, there is a decreased pCO2, which leads to alkalosis of the CSF and a depression of the central chemoreceptors.

Symptoms of Arterial Gas Embolism (5)

1. LOC 2. Confusion 3. Seizures 4. Cardiovascular Collapse 5. Death (5%)

How is high altitude pulmonary edema treated? (5)

1. Patients with mild cases may recover with bed rest. 2. Moderate cases can be treated with bed rest and supplemental oxygen if clinical monitoring is available. 3. Severe cases require oxygen and DESCENT! Use hyperbaric O2 therapy if available. 4. If oxygen or descent are unavailable, then nifedipine 10 mg every 4-6 hours or 10 mg followed by 30 mg slow release every 12 hours. 5. Inhaled beta-adrenergic agonist at a high dose can be used.

Symptoms of High Altitude Cerebral Edema (8)

1. Severe HA 2. Anorexia 3. Nausea 4. Altered LOC 5. Ataxia 6. Vomiting 7. Seizures 8. Coma

What are the two types of decompression sickness?

1. Type I: Type I decompression sickness is the non-systemic, MSK form. Type I is caused by free gas in the tissues and is manifested as pain in the extremities and joints (aka. the bends). Patients may also develop an erythematous or purpuric skin rash. 2. Type II: Type II decompression sickness is a systemic form. Type II is caused by free gas in the bloodstream and presents with severe neurologic symptoms, such as paresthesias, muscle weakness, and paralysis. If enough gas enters into the bloodstream and travels to the lungs, it can lead to obstruction of pulmonary vessels (aka. the chokes), presenting with chest pain, dyspnea, and cough.

The most significant and life-threatening dive injuries include (2):

1. arterial gas embolism (AGE). 2. decompression sickness (Type I and II).

Conditions associated with ruptured alveoli include (4):

1. arterial gas embolism. 2. pneumothorax. 3. pneumomediastinum. 4. subcutaneous emphysema.

Air travel can cause problems in patients with: (5)

1. compromised lung function. 2. coronary artery disease. 3. CHF. 4. OSA. 5. emphysema.

Diving disorders that require recompression therapy include (3):

1. decompression sickness type I. 2. decompression sickness type II. 3. arterial gas embolism.

Susceptible individuals to high altitude pulmonary edema often have a genetic component that present with (3):

1. decreased hypoxic ventilatory response. 2. increased hypoxic pulmonary vasoconstriction. 3. alterations in eNOS and endothelin.

In decompression sickness, the amount of nitrogen absorbed is determined by (2):

1. depth. An increased depth leads to an increased pressure. 2. duration. An increased duration leads to an increased time to absorb nitrogen.

The acute effects of hypoxia at 12,000 feet include: (5)

1. drowsiness. 2. laziness. 3. mental and muscle fatigue. 4. headache. 5. nausea.

How is high altitude cerebral edema treated? (2)

1. high altitude cerebral edema is treated with an immediate evacuation to a lower altitude. 2. Oxygen, bed rest, dexamethasone, and hyperbaric oxygen are used until descent.

Diving disorders that do not require recompression therapy include (15):

1. middle ear barotrauma. 2. external ear barotrauma. 3. inner ear barotrauma. 4. barosinusitis. 5. facial barotrauma. 6. nitrogen narcosis. 7. oxygen toxicity. 8. pneumothorax. 9. pneumomediastinum. 10. subcutaneous emphysema. 11. alveolar hemorrhage. 12. alternobaric vertigo. 13. barodontalgia. 14. gastrointestinal barotrauma. 15. avascular osteonecrosis.

High altitude cerebral edema is associated with (2).

1. severe acute mountain sickness. 2. high altitude pulmonary edema.

The acute effects of hypoxia at 18,000 feet include: (2)

1. twitchings. 2. seizures.

Medications for the treatment of acute mountain sickness are reserved for patients: (2).

1. who are known to be susceptible. 2. who must ascend quickly to high altitudes (i.e. rescue personnel).

What is acute mountain sickness?

Acute mountain sickness is a complication of altitude when travelers ascend suddenly to altitudes greater than 3000 m (9800 ft) above sea level, which causes acute hypoxemia and alkalosis. It is more common if a traveler fails to adequately acclimatize as higher altitudes are reached.

How can acute mountain sickness be prevented? (4)

Acute mountain sickness can be prevented by: 1. a gradual ascent with pauses for acclimation. This is the best method. Spend two nights at the same altitude for every 600-meter gain in altitude. 2. a high carbohydrate diet. A high carbohydrate diet can increase the respiratory quotient (due to R=1), resulting in a high alveolar pO2. A higher R diet can lead to increased ventilation to rid CO2. 3. acetazolamide. Acetazolamide is a carbonic anhydrase inhibitor, which induces bicarbonate diuresis and metabolic acidosis. Acetazolamide inhibits HCO3- production and prevents the production of CO2 from bicarbonate. Metabolic acidosis also results in hyperventilation, which increases alveolar pO2 and increases tissue capillary oxygen offloading by shifting the oxygen-hemoglobin dissociation curve to the right. 4. dexamethasone. Dexamethasone provides effective prevention almost equal to acetazolamide; however, it does not speed the acclimation process as well as symptoms may reappear if discontinued. As a result, acetazolamide is the drug of choice.

How does altitude affect the following mechanics of breathing: work and resistance?

Altitude leads to increased ventilation. Increased ventilation leads to increased work of breathing. With more active expiration, there is dynamic compression of small airways that are not supported by cartilage because expiration leads to a positive pressure in the thoracic cavity so that the outside pressure will be higher around the airway than inside the airway. As a result, the maximum airflow rate is reached, and airflow resistance is increased. There is also more turbulent air flow due to an increased ventilation rate, which also increases resistance and work of breathing as well.

What is an arterial gas embolism?

An arterial gas embolism is a A condition in which air bubbles enter the bloodstream and subsequently travel throughout the body, resulting from a rapid ascent from deep water that overexpands gas in the lungs too quickly. This is because pressure decreases, and gas volume increases. This overexpansion of gas in the lungs results in torn alveoli that release air into the pulmonary capillaries. Then, these air bubbles can travel through the arterial system and heart and may enter the brain, where they can cause symptoms of a stroke.

The acute effects of hypoxia at 23,000 feet include: (2)

An unacclimated person goes into a coma, followed by death.

What is the relationship between ventilation and oxygen consumption?

As oxygen consumption increases, ventilation increases linearly until a switch to anaerobic glycolysis occurs. When anaerobic glycolysis is triggered, then ventilation is stimulated more due to lactic acid production.

What is the relationship between oxygen consumption and work rate?

As work increases, oxygen consumption increases linearly until the maximum oxygen consumption rate has been reached. This is the maximum consumption where oxygen consumption cannot be increased any longer. At this point, an increase in work rate depends on anaerobic glycolysis.

What is the effect of altitude on ventilation?

At high altitude, there is a low pO2. A low pO2 stimulates the arterial chemoreceptors to send signals via the glossopharyngeal and vagus nerve to increase ventilation. However, ventilation is only increased about 1.65x normal because, although the central chemoreceptors do not respond to low O2, with an increase in ventilation, there is a decrease in pCO2. There is less CO2 diffusing into the CSF, which leads to a more alkaline pH in the CSF and the interstitial fluid of the medulla. This depresses the chemoreceptors, leading to less stimulation of the chemoreceptors for ventilation. As a result, altitude actually blunts the effect of a low pO2. Eventually, however, the pCO2 increases due to the increased work of breathing, which does aid the work of the central chemoreceptors.

What is the effect of altitude on pulmonary blood flow?

At high altitude, there is an increase in cardiac output, heart rate, and systemic blood pressure. This is most likely due to sympathetic stimulation secondary to peripheral chemoreceptor stimulation and increased lung inflation. Furthermore, at very high altitudes, hypoxic pulmonary vasoconstriction can occur. Receptors sense the alveolar pO2. When the alveolar pO2 is low, then blood is directed away from the regions of the lung because there is no gas exchange. This leads to vasoconstriction in those region. This can increase pulmonary artery pressure. In areas of increased blood flow, there is increased recruitment and distention, which can lead to pulmonary hypertension and lead to pulmonary edema.

What is the effect of high altitude on diffusing capacity?

At high altitude, there is an increase in pulmonary blood volume, which leads to an increase in surface area of the alveolar membrane. As a result, there is an increase in pulmonary artery pressure that causes recruitment and distension. All of this increases the diffusing capacity.

What is the effect of moderate depth on the mechanics of breathing in scuba divers?

At moderate depths, there is no problem for the work of breathing.

What is the effect of severe depth on the mechanics of breathing in scuba divers? How can this overcome?

At severe depths, gas densities cause an increase in airway resistance due to turbulent flow. As gas density increases, there is an increase in turbulent flow, which increases airway resistance. This can be overcome if nitrogen is replaced with helium at greater depths because helium is less dense than nitrogen.

What is the effect of exercise on alveoli at the top and bottom of the lung?

At the base of the lung, the alveoli are more inflated, although they can become compressed on expiration. However, the alveoli at the top of the lung ventilate better, as forceful expiration can increase expiration from these alveoli.

Breathing Air Altitude: Increases Barometric Pressure: pO2 in the Air: pCO2 in Alveoli: pO2 in Alveoli: Arterial Oxygen Saturation:

Breathing Air Altitude: increases Barometric Pressure: decreases pO2 in the Air: decreases pCO2 in Alveoli: decreases; This drop in pCO2 is due to the fact that as pO2 decreases, then hyperventilation occurs, which blows off CO2. pO2 in Alveoli: decrease Arterial Oxygen Saturation: decreases

Breathing Pure Oxygen Altitude: Increases Barometric Pressure: pO2 in the Air: pCO2 in Alveoli: pO2 in Alveoli: Arterial Oxygen Saturation:

Breathing Pure Oxygen Altitude: Increases Barometric Pressure: decreases pO2 in the Air: decreases pCO2 in Alveoli: decreases; This drop in pCO2 is due to the fact that as pO2 decreases, then hyperventilation occurs, which blows off CO2. pO2 in Alveoli: decreases Arterial Oxygen Saturation: decreases

How does the body acclimate to high altitude by day one?

By day one, there is renal compensation, with excretion of base and the conservation of H+ in response to respiratory alkalosis.

What is CO2 toxicity? What causes it?

CO2 toxicity is a condition in which there is too much pCO2 in the tissues. While CO2 toxicity is not an issue in scuba, it can become a problem in diving where equipment forces the diver to re-breathe the air, which increases alveolar pCO2. Above 80 mmHg CO2, the respiratory system can become depressed, and respiratory acidosis can occur. This can lead to a coma.

What is chronic mountain sickness?

Chronic mountain sickness occurs in individuals who remain at a high altitude for a long period time. In these individuals, the following occur: a high red cell mass and hematocrit, greater increases in pulmonary artery pressure, right heart enlargement, a fall in peripheral artery pressure, and congestive heart failure and death.

What is decompression sickness?

Decompression sickness is a a disorder in which nitrogen dissolved in the blood and tissues by high pressure forms bubbles as pressure decreases. When a diver descends deeper, atmospheric pressure increases. As a result, the blood and body tissues absorb a greater volume of gas, such as nitrogen. However, nitrogen is not metabolized by the body, so whatever nitrogen is absorbed must be expired by the body. When a diver ascends from depth, the nitrogen exits the body and is released. As the diver ascends, the pressure is decreased, and the absorbed nitrogen is released. If safety precautions are followed, then nitrogen will be released and cleared from body through normal respiration in a process known as off-gassing. However, if a diver ascends too quickly or bottom time is too long, and diver does not take proper precautions (such as safety stops), nitrogen can come out of absorption and form bubbles in the blood and body tissues that interfere with normal physiologic functions.

You are on a boat. A diver emerges with the bends. What do you do?

Do not recompress the patient, as they are often confused and combative. Rather, radio to the nearest hyperbaric facility, begin oxygen, give aspirin (325-975 mg) PO, and administer Ringer's lactate.

What is the effect of exercise on arterial pCO2?

During exercise, arterial pCO2 remains steady; however, when anaerobic metabolism occurs, arterial pCO2 can decrease. Anaerobic metabolism, with the production of lactic acid, can stimulate respiration at the peripheral chemoreceptors. This increase in ventilation can partially decrease the pCO2.

What is the effect of exercise on the Haldane effect?

During exercise, there is less oxyhemoglobin, which promotes the loading of CO2. This is because deoxyhemoglobin is a weaker acid, which will accept H+ better than oxyhemoglobin. As a result, bicarbonate will exchange out from the red blood cell in exchange for Cl- ions. This results in more CO2 being carried as bicarbonate and carbaminohemoglobin.

Exercise O2 Consumption: CO2 Production: Ventilation Rate: Arterial pO2 and pCO2: Arterial pH: Venous pCO2: Pulmonary Blood Flow (Cardiac Output): V/Q Ratio:

Exercise O2 Consumption: increase CO2 Production: increase Ventilation Rate: The ventilation rate increases and will match O2 consumption and CO2 production. Arterial pO2 and pCO2: There is no change unless strenuous exercise. Arterial pH: There is no change in moderate exercise; however, in strenuous exercise, arterial pH can decrease due to lactic acidosis when the anaerobic threshold is reached. This provides another surge for an increase in ventilation. Venous pCO2: With more CO2 produced in the muscles, then there is an increase in venous pCO2. This allows for a better diffusion gradient between the blood and the alveoli. Pulmonary Blood Flow (Cardiac Output): Pulmonary blood flow increases due to increased cardiac output. V/Q Ratio: The V/Q ratio increases because there is more ventilation versus blood flow, leading to a more even distribution of the V/Q throughout the lung.

What is the effect of exercise on pulmonary blood flow?

Exercise increases cardiac output due to an increase in heart rate. As a result, the mean left atrial pressure and the mean pulmonary artery pressure increase. This leads to a decrease in pulmonary vascular resistance via recruitment via the vessels in Zone 2 from intermittent flow to continuous flow and distension via the vessels in Zone 3. There is a decrease in pulmonary vascular resistance despite compression of the extra-alveolar vessels during expiration and the stretching of the alveolar vessels during inspiration due to an increased lung volume that both lead to an increase in resistance. This results in an improved pulmonary blood flow.

What is the effect of exercise on the ventilation-perfusion (V/Q) ratio?

Exercise increases ventilation more than that of blood flow. As a result, there is an increase in the V/Q ratio, leading to better matching. However, during more severe exercise, then ventilation increases more than perfusion, leading to an increase V/Q ratio.

High Altitude Alveolar pO2: Arterial pO2: Ventilation Rate: Arterial pH: Hemoglobin Concentration: 2,3-BPG Concentration: Hemoglobin-Oxygen Curve: Pulmonary Vascular Resistance:

High Altitude Alveolar pO2: Alveolar pO2 decreases due to a decrease in barometric pressure. Arterial pO2: A decreased alveolar pO2 leads to a decrease arterial pO2. Ventilation Rate: Because of a low arterial pO2, there is an increase in ventilation rate (hyperventilation). Arterial pH: With hyperventilation, there is an increase in arterial pH (respiratory alkalosis). Hemoglobin Concentration: Hemoglobin concentration is increased due to increased EPO. 2,3-BPG Concentration: The concentration of 2,3-BPG increases. Hemoglobin-Oxygen Curve: The hemoglobin-oxygen curve shifts to the right, leading to a decreased affinity of hemoglobin for oxygen. Pulmonary Vascular Resistance: Altitude increases pulmonary vascular resistance due to hypoxic vasoconstriction.

What is high altitude cerebral edema?

High altitude cerebral edema is a more severe form of acute mountain sickness in which the passage of fluid occurs from the intravascular to the extravascular space, particularly in the white matter. This leads to a vasogenic edema. Vasogenic edema leads to alterations in the blood brain barrier, including inhibition of CSF from shifting out of the cranium due to CSF volume buffering and increased ICP.

What is the leading cause of death at high altitudes?

High altitude cerebral edema is the leading cause of death at high altitudes.

How is the hypoxic ventilatory response affected by high altitude pulmonary edema?

High altitude pulmonary edema blunts the hypoxic ventilatory response. Normal stimuli increase the respiratory rate include CO2, O2, and acidemia. However, at higher elevations with lower oxygen pressures and the same carbon dioxide production, hypoxia will dominate as the primary respiratory stimulus, leading to a decrease in alveolar oxygen that leads to an increase in breathing rate.

What is high altitude pulmonary edema?

High altitude pulmonary edema is a severe complication of mountain sickness due to worsened arterial hypoxemia from lower concentrations of O2 at higher altitudes. This leads to increased pulmonary artery pressure that leads to downstream capillary stress injury and possible pulmonary venoconstriction. Gas exchange in this condition is worsened by non-cardiogenic pulmonary edema due to a flow of fluid from the intravascular space to the extravascular space. There is also a delay in O2 diffusion, as the alveolar walls are thicker and more edematous, reduced lung volumes, reduces diffusion capacity, and small airway bronchoconstriction.

What is the mainstay of diving injury treatment?

Hyperbaric therapy is the mainstay of diving injury treatment.

How is acute mountain sickness treated? (6)

Mild cases are usually self-limited and do not require treatment. However, if treatment is required, then: 1. discontinue ascent, rest, and limit exertion. 2. for moderate cases, administer acetazolamide. 3. administer acetaminophen for headaches. 4. administer prochlorperazine, a ventilatory stimulant, for nausea. 5. administer supplemental oxygen if available. 6. add dexamethasone in severe cases.

What is the effect of exercise on alveolar ventilation?

Less strenuous exercise increases tidal volume to increase ventilation with no major change in dead space.

What is nitrogen narcosis?

Nitrogen narcosis is a state in which there is increased N2 dissolved freely in the fatty substances of the membranes of the neurons, which alters ionic conductance through the membranes and reduces neuronal excitability. It can occur one hour after diving. By 120 feet, patients present with joviality. By 150 to 200 feet, patients present with drowsiness. By 200-250 feet, patients present with low strength.

What is oxygen toxicity? What causes it?

Oxygen toxicity is a condition in which there is an excess of oxygen dissolved in the blood at higher pressures. Hemoglobin, once maxed, cannot prevent this high pO2, which leds to a high tissue pO2. Oxygen is toxic to tissues, especially the brain. As a result, seizures and a coma can result within 30 to 60 minutes. Other symptoms include nausea, twitching, dizziness, and disorientation.

What causes oxygen toxicity?

Oxygen toxicity is caused by reactive oxygen species. Oxygen can be converted into reactive oxygen species that can damage lipid, protein, and DNA in cells. Normally, there are detoxification enzymes in the cell to prevent damage; however, they are overcome by the high amount of reactive oxygen species being generated at depth. At high tissue pO2, radicals that are formed react with lipid in nervous tissue, causing damage.

What is the effect of breath-hold diving on gas exchange in the lungs?

Prior to breath-hold diving, a diver hyperventilates, thereby increasing the partial pressure of oxygen in the alveoli and decreasing the partial pressure of CO2. However, by 33 feet, the lung volume decreases, and the pressures increase. This doubles the total gas pressure. Further, alveolar pO2 increases, so there is no problem with diffusing oxygen due to a large pressure gradient between the alveolus and blood. The problem however is moving pCO2 out of the blood and into the alveolus. Therefore, the alveolar pCO2 increases, resulting in a situation where it is difficult to move CO2 out of the blood and into the alveolus. An increase in CO2 in the blood leads to a respiratory acidosis

What is the effect of altitude on diffusion?

Regarding diffusion, the partial pressure gradient for O2 is decreased at high altitude due to a low alveolar pO2. This means that the pressure gradient is decreased for diffusion, which means that there is decreased diffusion of oxygen across the respiratory membrane. However, this is partly offset by: 1. increased cardiac output. There is more blood entering the system per minute, which aids in picking up oxygen and delivering it to tissues. 2. increased pulmonary artery pressure. This increases surface area for diffusion.

What is the effect of altitude on ventilation-perfusion?

Regarding ventilation-perfusion (V/Q), there are small improvements in the V/Q ratio. This could be due to hypoxic pulmonary vasoconstriction.

What is the diving reflex?

The diving reflex states that when the head is immersed, heart rate decreases, and systemic vascular resistance increases. This decreases the work of the heart, but severely limits perfusion to the systemic vascular beds with exclusion to the heart and brain.

What is the problem with diving?

The problem with diving that pressure increases with descent. The body's tissues do not compress, but the gasses do. According to Boyle's law, as the pressure increases, then the lung volume decreases. Furthermore, according to Dalton's law, as the total pressure increases, the partial pressure of gases increases. Lastly, by Henry's law, as the partial pressure of a gas increases, the amount of gas dissolved in the body increases.

What is the effect of exercise on the mechanics of breathing?

The work required for breathing increases. This is because a larger tidal volume increases work to overcome to the elastic recoil of the lung and chest wall. While the greater elastic recoil of the lungs due to larger volumes at the end of expiration makes it easier to expire, high airflow rates lead to an increase in airway resistance, as it results in more turbulence and airway compression during active expiration.

What is the effect of exercise on diffusion rate?

With exercise, the lungs are perfused and ventilated more. With increased perfusion and ventilation, the surface area for perfusion increases, which leads to an increase in perfusion. Furthermore, with an increase in blood flow, there is an increase in diffusion capacity. There is less of an effect of perfusion limitation and allows the maintenance of the partial pressure gradient. However, the blood entering the pulmonary circulation could have a lower pO2 and a high pCO2, which could result in a large pressure gradient and thereby increase diffusion.

What is the effect of diving with scuba gear on the respiratory system?

With scuba gear, the gas pressure in the lungs is close to ambient; however, the advantage is that expired gas is released into the water. As a result, there is no accumulation of CO2. HOwever, the problem with scuba diving is related to gas densities and partial pressures.

How does the body acclimate to high altitude within two to five days?

Within two to five days in high altitude, the bicarbonate level decreases within the CSF. As a result, the central chemoreceptors are no longer depressed, leading to the full force of hypoxemia stimulation at the peripheral chemoreceptors. As a result, hyperventilation increases. Furthermore, by days two through five, there is alleviation of cerebral edema and CNS symptoms and well as cardiac output, heart rate, and systemic blood pressure return to normal due to a decrease in the sympathetic system. However, hypoxic pulmonary vasoconstriction and pulmonary hypertension persist. Over the long term under extreme conditions, this results in right ventricular hypertrophy and failure under extreme conditions.

How does the body acclimate to high altitude within two weeks?

Within two weeks at high altitude, there are changes in blood volume due to an increase in red blood cell production. However, to maximize blood volume, this will take months. As a result, Hb increases from 15 to 20 g/dL, blood volume increases by 20-30%, and 50% more hemoglobin is circulating. However, this increase in circulating volume increases blood viscosity and ventricular workload.

Exercise shifts the oxygen-hemoglobin dissociation curve to the _______ because (4).

a lower pO2, increased temperature, increase pCO2, and increased H+

Before flying, patients with compromised lung function should undergo _____.

a pre-flight assessment. The flight cabin is maintained at a pressure around 8,000 feet. So, a pre-flight assessment is used to determine the need for in-flight oxygen with a goal of maintaining PaO2 of ≥50 mm Hg.

Acute mountain sickness is most common with _____.

a rapid ascent to altitudes greater from 10,000 feet

With an increase in altitude, there is a ______ in inspired pO2.

decrease

With an increase in altitude, there is a ______ in barometric pressure.

decrease * This is because the total barometric pressure is proportional to the weight of the air above it. ** This has a dramatic effect on the inspired effect on the inspired pO2. The inspired pO2 is the pO2 in the conducting airways.

Altitude __________ the work of the right ventricle.

increases

As oxygen consumption increases, ventilation _________.

increases * This increase in ventilation occurs immediately after exercise. Ventilation works to maintain a normal pO2, pCO2, and pH, and these blood gases are maintained unless the exercise is very strenuous.

In the treatment of acute mountain sickness, avoid _____.

narcotics

In high altitude pulmonary edema, inhomogeneous alveolar infiltrates are initially found _______.

on the right side

If patient has evidence of bullous lung disease due to emphysema, there is an increased risk of ________.

pneumothorax

Acetazolamide shifts the oxygen-hemoglobin curve to the ______.

right * As a result, acetazolamide increases oxygen off-loading in the tissues.

If a patient is considered high risk for air travel, then the goal pO2 should be ______.

wherever the patient is stable

High altitude pulmonary edema is commonly seen in _______.

young persons who ascend rapidly between 2 to 4 days after arrival to a high altitude