40% HAVE A PFO (PATENT FORAMEN OVALE) – DO YOU?

 

However, people with a PFO have an opening between the right and left upper heart (atria) that can be small in some people and larger in others. No matter what the size of the hole while resting, it becomes stretched and larger when the person sits or stands from a lying position, lifts something heavy, or bears down, as if having a bowel movement.  

 

The incidence of PFO decreases with age, declining from 34% in people between the ages of 0 and 29 years to 25% in people between the ages of 30 and 79 years to 20% in people between the ages of 80 and 99 (1). However, the average size of the PFO increases with age from 3.4 mm during the first 10 years of life to 5.8 mm during the 10th decade of life (1). Even though up to 40% of the adult population have a PFO, little research has examined its impact on normal physiological processes. 

 

At the end of a normal inspiration during diastole, the PFO allows a potentially significant amount of blood to bypass the lungs especially during exercise, at high altitude, and in patients with pulmonary hypertension. This does not occur with every heart beat.  That portion of the blood that does not go through the lungs will:

1) not pick up oxygen and get rid of carbon dioxide causing problems at rest and high altitude;

2) not be filtered of blood clots or air bubbles.  Consequently, unfiltered clots and air bubbles can go directly to the brain (STROKE), heart arteries (HEART ATTACK), eye (BLINDNESS), migraines with aura, kidney, any other organ;

3) not get cooled, resulting in a higher core temperature that results in an even lower oxygen level.

For many years only the issue of unfiltered blood clots causing a stroke was used to decide how to treat a patient with a PFO because the other important physiological consequences were not considered: including hypoxia, carbon dioxide retention, higher core temperature, and unfiltered air bubbles.

 

THE LARGER THE HOLE, THE WORSE THE PROBLEMS

 

REDUCED GAS EXCHANGE EFFICIENCY – less oxygen acquired and more carbon dioxide retained for the person with a PFO for two reasons: 1) simply less blood flow to the lungs; 2) gas exchange is less efficient (2). The size of the hole matters and not just having a PFO.  The larger the hole, the less oxygen is picked up. Older patients (>65) with PFOs who also have heart failure with or without pulmonary hypertension have lower blood oxygen levels (SaO2) at rest (3).  Surgical closure of the PFO improves arterial oxygenation at rest and during exercise, thus showing that blood flow through a PFO definitely has a measurable impact on gas exchange (4). 

 

% OXYGEN SATURATION ( SaO2%) refers to the amount of oxygen picked up by red blood cell’s hemoglobin in the lungs.  It is measured by a device called a pulse oximeter (pulse ox) put on a finger. The normal range is 97% to 100%. Below 95% is considered low for people without diseases and oxygen is usually administered if the level is about 92% or below.  The normal range for a person with severe Chronic Obstructive Pulmonary Disease is 88%-92%. 

 

CONSEQUENCES OF HYPOXIA – LOW BLOOD OXYGEN 

1). Shortness of breath, fatigue, chest pain, confusion, headache, rapid heartbeat that results in less volume of blood pumped by the heart (decreased stroke volume).  Blood levels below 80% can compromise the brain and heart. Continued low oxygen levels may lead to respiratory or cardiac arrest and loss of consciousness.

2). Constriction of small pulmonary arteries and dilatation of systemic arteries

3). Hypercoagulable state (increased by two-fold to eight-fold) causing clots is caused by acute low-pressure hypoxia at high altitude (5).

4). Higher rate of death and morbidity for outpatients with pneumonia when their oxygen saturation is less than 90% (6).

5). Jet Lag is caused by this fall in oxygen saturation and altitude sickness.

 

 

BODY TEMPERATURE

When the core temperature rises in a person without a PFO, the body responds by taking deeper breaths more rapidly to cool down the blood in order to maintain a constant brain temperature.

 

PFO patients have a higher core temperature at rest and during exercise (about 0.4 degrees C) because some of the blood does not go through the lungs to get cooled. This higher temperature results in an even lower oxygen level (because of a right-shifted oxyhemoglobin dissociation curve). The SaO2% is reduced by 1.5% – a significant amount (2).  Therefore, on a hot day in the sun, these patients can become fatigued and lethargic within minutes due to the higher core temperature and lower oxygen level without any significant blood pressure reduction.  They have a higher risk for heat exhaustion and heat stroke.  These patients feel better when they put at least their feet in a cooler body of water – pool, lake, ocean, even cool water in a bathtub.  Air conditioning may help, but some have had difficulty cooling down when given cool air to breathe.

 

HUMIDITY

Adding humidity to the air DECREASES the oxygen molecules because the water molecules displace oxygen and the other gases.  The total pressure of air at sea level is 760 mm Hg (mercury) with or without humidity.  Nitrogen is the most abundant gas comprising 79% of air’s concentration, followed by oxygen at 20.93% and carbon dioxide at 0.03%.

 

The concentration of oxygen in DRY air is calculated by multiplying 20.93% times 760 mm Hg = 159 mm Hg. This is the concentration of oxygen that enters the mouth and nose.  As the air descends into the lungs where it gets humidified the concentration of oxygen decreases even more.  At the level of the trachea of the lungs it is 149 mm Hg.  At the alveoli, where gas exchange actually occurs, the oxygen concentration is 105 mm Hg because of the higher humidity at that level.  When the atmospheric air is HUMID, there is even less oxygen in it and therefore less oxygen that enters the mouth and nose.  As that air descends to the alveoli, the oxygen content is much lower compared to the DRY air example.     

 

A person with a PFO will have a lower blood oxygen saturation in humid weather.  If it is hot and humid, the person with a PFO has a much harder time breathing and fulfilling the body’s needs of oxygen. 

 

 

HIGH ALTITUDE reduces breathing response, decreases the ability to oxygenate the blood and increases the susceptibility to Acute Mountain Sickness.  A study (7) done on 21 healthy 20 year old subjects (11 with relatively small PFO) at a research facility at Mt. Chacaltaya, Bolivia, 5,260 m = 17,257 feet showed that gas exchange got worse for all people with or without a PFO when they were taken directly up to this high altitude.  The oxygen saturation was about the same for those without or with a PFO: 67% vs 66%, respectively.   For people without a PFO the oxygen saturation improved to 76% after 16 days of acclimatization because more oxygen is taken in by the lungs (increased alveolar ventilation).

 

But people with a PFO did not attain acclimatization after 16 days – both at rest or while exercising – and were still suffering from Acute Mountain Sickness (oxygen saturation = 70%).  Symptoms of Acute Mountain Sickness include headache, anorexia, insomnia, breathlessness, and unsteady gait. They also had a higher risk for high altitude pulmonary edema (fluid in lung), stroke, heart attack, and damage to other organs. 

 

Deep Breathing: One way to partially compensate for a decreased intake of oxygen at high altitudes is to slow down your breathing rate but increase the depth of your breaths. Instead of breathing quick and shallow and only in your lungs, breathe slowly and deeply and inhale until your stomach expands.

 

People who are born and live at high altitude have the same prevalence and sizes of PFOs as those who are low-altitude natives. Selective adaptation might have eliminated PFOs for those living at high altitude – but it did not. Tibetans, who thrive at altitudes over 4400 meters (14,435 feet) and whose ancestors have lived at high altitudes for thousands of years, have two gene variants (EGLN1 and PPARA) that help them use oxygen more efficiently with less hemoglobin than people who live at low altitudes – a process that may involve nitric oxide (8).

 

The following lists the ALTITUDE and % OXYGEN SATURATION for people WITHOUT a PFO.  

0 feet     0 meters  97%

5,000 ft    1525 m  94%

6,000 ft    1825 m  93% Boeing 787 cabin altitude

8,000 ft    2440 m  91% Boeing 737 cabin altitude

8,000-10,000 ft  2440-3050 m  91% – 88% Learjet cabin altitude

10,000 ft  3050 m  88%  

12,000 ft  3660 m  84% 

13,120 ft  4000 m  80%

17,257 ft  5260 m  67% Mt. Chacaltaya, Bolivia

19,700 ft  6000 m  65%

26,250 ft  8000 m  <50% DEATH ZONE

 

The % OXYGEN SATURATION for people WITH a PFO is lower.  

 

People with a PFO traveling in a Learjet (cabin altitude 8,000-10,000 feet), Boeing 737 (cabin altitude 8,000 feet), or a Boeing 787 (cabin altitude 6,000 feet), will have an % OXYGEN SATURATION lower than 88%-91%, 91%, 93% respectively, and below 95% is considered low. 

 

 

AIR FLIGHT 

US Federal Aviation Regulations state that pressurized cabins must provide a cabin altitude of not more than 8000 feet at the maximum operating altitude of the airplane (FAA, 1996), so that the partial pressure of oxygen be maintained at 0.17–0.15 at sea level.  Cabin altitude measurements by 28 airlines range from sea level to 8,915 feet. 

 

The Boeing 737’s cabin altitude can climb to 8,000 feet while the aircraft’s actual altitude is 41,000. Newer aircraft such as the Boeing 787 are designed to have lower cabin altitudes of 6,000 feet.  At 35,000 feet in a Learjet, the cabin altitude may be 8,000 to a maximum of 10,000 feet. There is less oxygen in the air at higher altitudes and our ability of get enough oxygen decreases.  Alveolar oxygen tension decreases to 65 mm Hg at 8000 feet that reduces arterial oxygen tension to 60 mm Hg in healthy individuals (9).  Patients with chronic hypoxia may have a greater reduction in SaO2 when they reach high altitude than those with healthy lungs.  Any small reduction in the oxygen content of the air in the cabin results in a significant decrease in the SaO2 because of the oxyhemoglobin dissociation curve.  This is even worse for those with PFOs.  

 

The cabin pressure is mechanically increased by routing compressed air (“bleed air”) from the turbine engines to the air conditioning system.  The cabin pressurization and ventilation is controlled by opening and closing of outflow valves via the pressure controller switch. This system pumps air into the aircraft that is adequately sealed to limit the rate at which this air escapes from the airplane cabin.  Cabin altitude is a better physiological indicator than cabin pressure.  

 

People are most comfortable when the plane climbs or descends at a rate of 500 feet per minute or less. Faster rates are uncomfortable and can cause painfully blocked ears and sinuses, and, in extreme cases, incapacitation. A turbine aircraft typically climbs and descends several thousand feet per minute. The pressure controller regulates the cabin altitude and varies the pressure at rates much lower than the aircraft’s actual altitude. For example, the cabin altitude climbs to 8,000 feet (taking 16 minutes at 500 feet per minute) while the aircraft actual altitude climbs to about 40,000 feet (at an average 2,500 feet per minute in the same 16 minutes).

 

There are two types of pressure control systems. The completely automated one requires the pilot to enter only the destination field elevation and then it schedules the timing and rate of cabin climb or descent. Older systems require the pilot to set the rate of a cabin climb/descent. After takeoff, the controller is set according to cruise altitude, and prior to descent it is adjusted to a level appropriate to the landing field elevation. This setting is usually 500 to 1,000 feet above the airport elevation.

 

If sudden cabin depressurization occurs in an aircraft like a Learjet flying at 35,000 feet, the pilots and passengers may initially experience a brief euphoria and then have as little as 5 to 12 seconds of useful consciousness to put on their oxygen masks. Following this brief period, without supplemental oxygen, their cognitive and motor skills diminish, leading to incapacitation, often with fatal consequences.

At 35,000 feet in a Learjet, the cabin altitude may be 8,000 to a maximum of 10,000 feet. If the cabin altitude rises above 10,000 feet, a device developed by NASA makes a chirp and the LED flashes. If the cabin altitude exceeds 12,500 feet, a 30-minute timer starts, and if it stays above 12,500 feet but below 15,000 feet for longer than 30 minutes, an un-mutable, sustained alarm will sound and the LED will flash. This same alarm mode will be in effect if the aircraft cabin pressure exceeds 15,000 feet for any period of time.

 

SaO2s for 84 passengers not tested for PFO, aged 1–78 years were recorded by pulse oximetry at ground level and during air travel on 10 different airlines at altitudes ranging from 27,000 to 37,000 feet (10).  There was a significant reduction in oxygen saturation in all passengers travelling long haul and short haul flights that lasted 1 hour or more. The mean SaO2 for all flights at ground level was 97% [93%–100% +/- 1.33] and at cruising altitude 93% [85%–98% +/-2.33]. Fifty-four per cent of passengers had SaO2 of 94% or less at cruising altitude for which more than one-third of respiratory physicians would prescribe supplementary oxygen (11).  No individual had severe cardio-pulmonary problems, and no one required permission from their doctor to fly. Their smoking status was unknown.     

Low SaO2 (hypoxia) increases the risk for DVT (Deep Venous Thrombosis) because it increases coagulation, dilates blood vessels and increases capillary permeability.  These blood clots in the legs can break off and go to the lungs in a person without a PFO or can go to the brain, heart, or any other organ in a person with a PFO.   Other risk factors for causing DVT are reduced blood flow (immobility in the aircraft), dehydration, and damage to blood vessels.

People with a PFO traveling in a Learjet (cabin altitude 8,000-10,000 feet), Boeing 737 (cabin altitude 8,000 feet), or a Boeing 787 (cabin altitude 6,000 feet), will have an % OXYGEN SATURATION lower than 88%-91%, 91%, 93% respectively, and below 95% is considered low. 

ALTITUDE DECOMPRESSION SICKNESS