Clinical Applications of Gas Laws Workshop

Brain

High altitude cerebral edema: ataxia, fatigue, mental status, progressive decline in cognitive/mental function, declining level of consciousness, impaired coordination and slurred speech

Lungs

High altitude pulmonary edema: Occurs 2-4 days after climb and may accompany high altitude cerebral edema

Hyperventilation in room air vs. hyperventilation in high altitude

Hyperventilation in room air: PACO2: Decrease CO2: decrease O2: either stay the same or increase hyperventilation in high altitude: CO2: decrease O2: decrease

Treatment for High Altitude Pulmonary Edema (HAPE)

Treatment: • Decrease in pulmonary artery pressure • Decrease in physical activity, keep warm and start descending • Hyperbaric chamber (some use CPAP machine if chamber is unavailable) Pharmacological interventions (mainly aimed at targeting vascular tone): • Nifedipine (calcium channel blocker) • Sildenafil (PED 5 inhibitor): PED5 normally causes vasoconstriction *Both of these decrease BP back to normal, so vascular leakage will stop Prevention: • Gradual climb: give yourself time to acclimatize ( "CLIMB HIGH, SLEEP LOW") • Pre-acclimatization: live in moderate high altitude for a few weeks before the main climb or simulate a hypoxic environment

What is the estimated PAO2 at the highest elevation climbed? PAO2 = (Atm pressure - H20 pressure) * FiO2 - (PACO2 / R)

PAO2 = (Atm pressure - H20 pressure) * FiO2 - (PACO2 / R) assume: P Atmosphere is 500 mmHg R= 1 PACO2 = 40 mmHg H2O pressure= 47 FiO2= 21 (500- 47) * 21- (40/1)= 9473

What are the different high-altitude sickness

-Acute Mountain Sickness (AMS) -High Altitude Pulmonary Edema (HAPE) -High Altitude Cerebral Edema (HACE)

Given the hypobaric environmental challenge, what major organ systems are involved in the etiopathogenesis of the complaint?

-Brain -lungs -kidneys

Case #1 • A 25-year-old student and his companions drove from sea level to nearly 8000 ft (2440 m) in the Sierra Nevada Mountains of California. They then hiked to 9,000 ft (2,740 m), where they spent their first night. The next day, they continued to 11,000 ft (3,350 m), and on the third day, after considerable exertion digging a snow cave, they camped at 12,400 ft (3,780 m). • That night, the student developed a mild cough but otherwise was asymptomatic. On the morning of the fourth day, approximately 60 hours after leaving sea level, the group attempted an ice-climbing route. During the climb, the student noted considerable fatigue, shortness of breath, hyperventilation, mental confusion and he was unable to keep up with his climbing partners. By early afternoon, they abandoned the climb and began the descent. The student was, by then, extremely fatigued and reported an intense headache. His cough increased, and shortly thereafter, he began coughing up thin straw-colored fluid. He continued the descent unaided but with some difficulty. Finally, after approximately 12 hours of descent, the party arrived at their car. After driving to 4000 ft (1220 m), the student felt markedly improved but still exhausted.

-The first paragraph tell us that the patient is at high altitude High altitude= air is less pressurized -His symptoms are occuring due to lack of O2 being perfused to the organs especially the brain *In the brain, CO2 (this normally constricts) is an important regulator -This patient is hyperventilating: meaning they are breathing out a ton of CO2~ this causes the brain to dilate-> cerebral edema (makes sense why he has an intense headache) -Thin straw-colored fluid indicates blood -blood is leaking into the lung alveoli and cause the patient to cough it up

• What is the cause of the widened A-a gradient?

Aa gradient= measures the difference between the oxygen concentration in the alveoli and arterial system -a widened Aa gradient is from the pulmonary embolism which happened from the deep vein thrombosis -blood vessel Is blocked causing less perfusion to the tissues

Pressure-solubility relationship: basic principle

As you increase the pressure of a gas, the collision frequency increases and thus the solubility goes up, as you decrease the pressure, the solubility goes down

High altitude effect on chemosensory feedback

At high altitude, low arterial PO2 stimulates the Carotid bodies/peripheral chemoreceptors, resulting in an increase in alveolar ventilation. Acutely, at high altitude, the main drive for ventilation changes from CO2 on the central chemoreceptors at sea level, to a PO2 drive of the peripheral chemoreceptors, and hyperventilation ensues Carotid bodies -peripheral chemoreceptors Brain -central chemoreceptors

• Acutely, altitude-induced hyperventilation results in respiratory alkalosis, resulting in an increase in arterial pH • How does this happen?

CO2 + H2O ⇌ H2CO3 ⇌ H+ + HCO3 -

Case #3 Continued • Physical exam reveals an obese woman with a BMI of 40 in moderate respiratory distress. Her HR is 117/min and regular, RR is 25/min, BP is 139/81 mmHg and Temp is 37.8C. Lung auscultation reveals a clear lung field. Extremities show signs of cyanosis, with no clubbing or edema

Lung auscultation reveals a clear lung field -this tells us that she can ventilate but cannot perfuse additional tests: Arterial blood gas (ABG)

Treatment for High Altitude Cerebral Edema (HACE)

Onset of cerebral dysfunction • Mistaken for exhaustion • Occurs ~2500 meters after symptoms of AMS Symptoms • Ataxic gait, decrease mental function, decrease consciousness, slurred speech, confusion Treatment • Descent and hyperbaric O2 chamber • If unconscious, secure the airway and keep it open to maintain air flow

ABG results from case 3 • Arterial blood gases reveal a PaO2 of 61 mmHg and a PaCO2 of 32 mmHg on room air. Arterial blood PH is 7.57 and the calculated A-a gradient is 37 mmHg. A gram-stain sputum specimen exhibits normal finding. Chest X-ray reveals clear lung fields, except for a small peripheral infiltrate in the right lower lobe. CT pulmonary angiogram reveals an embolus in the right lower lobe

PaO2 is 61 (this should be 100) Aa gradient= 39 mmHg (100-61) Normal Aa gradient= 5-15 mmHg pH is 7.57: alkalanic -why high? blow off CO2 b/c of hyperventilation CT pulmonary angiogram: this can detect ventilation-perfusion mismatch

Case #3 • A 41-year-old office secretary recently drove from Alaska to Florida to start a new office job. The trip took about 90-hours of driving, with a few short breaks in between. Three days after her arrival, she started experiencing right-sided chest pain, cough, and dyspnea. She drove herself to the ER after experiencing the right-sided chest pain. At the ER, she developed mild distress, with a RR of 24/min, severe shortness of breath and mild coughing. She denies having been treated for respiratory problems and her overall medical history is negative. Her only medications are oral contraceptives and warfarin. Her family history is negative for asthma and cardiovascular disease. She reports having missed her required dose of warfarin since making the move to Florida

Plausible diagnosis: -Deep vein thrombosis which becomes a pulmonary embolism -MI

Pressure-volume-density relationship

this means that density decreases with increasing volume i.e. pressure is directly proportional to the density of a substance or an increase in pressure will increase the density and vice-versa Essentially: Increasing pressure will increase the gas density and decrease the volume -decreasing pressure will decrease the gas density and increase the volume

From case 3, What roles do the missed medications play in the etiopathogenesis of the complaint?

warfarin is a vitamin K antagonist which prevents blood clots

Decompression Sickness (Dysbarism)

• High barometric pressure causes compression of gases • As the diver comes back up to the surface, surrounding pressure decreases, and therefore, gas volume increases/expands • Due to the sudden release of surrounding pressure, N2 comes out of tissues very rapidly and expands (comes out of solution) • There will be no time for the N2 to be efficiently eliminated from the body since the only place it can be eliminated from is at the lungs • The N2 will escape the solution and form bubbles (emboli of gas)

Treatment for Acute Mountain Sickness (AMS)

• No further ascending • Decrease physical activity (no carrying back packs or extra weight) • Most will acclimatize by 24-48 hours (will compensate by lowering bicarbonate levels with urination) • Symptomatic relief: aspirin, acetaminophen • Start descending until they get better • Can give supplemental Oxygen (2-4 L/min) for about 15-20 minutes every 2 hours (can be alternative to descent if coming back down is not an immediate possibility) • Hyperbaric oxygen chambers: there are portable/inflatable chambers that can help with recovery *be careful giving aspirin b/c of it antiplatelet effect

Kidneys

➢ High hematocrit and an increase in EPO occurs with high altitude stemming from kidney stress in subchronic/prolonged time domains ➢ This is referred to high altitude-induced adaptive polycythemia