It wasn’t until over a week later, finally on the way to the doctor after days of delay, that I admitted it might be blood clots in my lungs. Sure enough. But at first, in the days following our return flight to New York in the flight levels, I thought the long hours on oxygen or decompression might explain my symptoms. I researched absorption atelectasis and the chokes.

Absorption atelectasis

Alveoli provide extremely efficient oxygen transfer from inhaled gases into solution in the blood in the surrounding capillaries and then into chemical bond with hemoglobin. If those inhalations contain little else but oxygen, and if their pressure is substantially reduced by high altitude, then there is a tendency for the alveoli to collapse. The positive pressure oxygen systems used by military pilots in unpressurized aircraft at high altitudes counteract this tendency. On our return trip at FL230, we were using the type of continuous flow system that is standard in light aircraft, approved for use up to about 25,000 feet. These masks have rebreather bags that help conserve oxygen by mixing some exhaled carbon dioxide and water vapor into inhalations. The presence of those gases in inhalations would also counter collapse of alveoli by tending to hold the overall pressure higher even when the oxygen partial pressure decreased rapidly due to absorption into the blood.

I learned atelectasis is a risk in such flights, but began to look elsewhere after a few days. The condition was not improving, and I had flown similar profiles before, albeit not as long.

The chokes

Breathing difficulties, “the chokes”, are among the most serious effects of sudden decompression. Divers who surface too quickly experience a rapid decrease in gas pressures which can lead to the release of super-saturated nitrogen in the form of bubbles trapped inside tissue. In the more common “bends”, the bubbles are trapped in joint tissue, causing pain upon use of the joint. When reproduced in experimental animals, the chokes reveal nitrogen bubbles trapped in pulmonary arteries, leukocytes surrounding them, then development of lung edema.

I contacted medical personnel at the closest facility with a hyperbaric chamber to discuss this possible diagnosis and to see if they thought recompression would be appropriate in my case. As we talked through the history of my symptoms, it quickly became clear that it was not the chokes. My decompression from sea level to FL230 had occurred slowly and resulted in no symptoms at altitude. My recompression had already occurred in the descent for landing days before.

it was now over a week since I first showed the symptoms of “shortness of breath” on exertion, pushing the airplane into the hangar in Oklahoma. That was before the high altitude legs. I had been in relatively good condition immediately before the appearance of that symptom. It was getting progressively worse, not better. I was beginning to notice my nailbeds turning pale with mild exertion, such as slowly climbing a gentle hill. I sometimes had to sit down to get my respiration rate to slow down after climbing stairs. Something had changed radically and was continuing to change.

Deep vein thrombosis (DVT)

In DVT, clots form in the veins of the legs, most commonly in the calves, and most commonly in the left leg. One theory for the higher frequency in the left leg cites the routing of the left common iliac vein behind the right common iliac artery, where it can be compressed against the lumbar spine. This phenomena and theory are referred to as the May-Thurner Syndrome, in honor of R. May and J. Thurner, who first described it in 1957.

Eight years previous I had been diagnosed and treated for deep vein thrombosis (DVT) in my left leg. My recovery appeared to have been complete. There had been no recurrence of swelling in the leg. The presumed cause had been determined to have been very long flight legs in a survival suit, while limiting fluid intact; I had subsequently been persuaded to stop doing the transatlantic flights that required those conditions. In addition, in the years immediately following the DVT, I had been careful to keep hydrated on longer flights, to move my legs regularly, and to watch for any signs of swelling. As time passed with no sign of recurring problems, I had grown lax, limiting fluid intake on long legs to avoid the need to urinate and failing to move my legs regularly.

DVT can also lead to complications in the legs referred to as chronic venous insufficiency (also known as post-thrombotic syndrome). This condition is characterized by pooling of blood, chronic leg swelling, increased pressure, increased pigmentation or discoloration of the skin, and leg ulcers known as venous stasis ulcer. Since my 2001 DVT, I have had mild post-thrombotic symptoms — splotchy red discoloration on the skin of my left ankle, and occasional soreness in my left calf. But these mild post-thrombotic symptoms had not changed recently, so initially I did not consider my new shortness of breath symptom related to my earlier DVT.

I walked into my internist’s office without an appointment early on the day after Labor Day 2009, having finally decided it was time to seek medical help. I was there before he was. When he came in and heard the symptom, he immediately examined me and ordered an EKG. Judging by a change in the EKG, added to the account I gave him of the flights to and from Oklahoma, he came up with a diagnosis of pulmonary emboli within minutes and ordered an ambulance to take me to the nearest emergency room, where I was put on oxygen and a chest CT scan revealed extensive clots in the pulmonary arteries in both lungs. I was injected with a form of heparin, Enoxaparin sodium (manufactured and marketed by Sanofi-Aventis under the tradename Lovenox), to counter the formation of further clots and allow my body opportunity to begin to clear existing clots. I was also started on longterm warfarin to reduce clotting factors and lower the likelihood of further clot formation.

Pulmonary emboli

Blood clots that detach from the place where they originate and travel through the circulatory system to lodge elsewhere are termed emboli. If they lodge in the blood supply to the lungs, they are termed pulmonary emboli (singular: embolus). Almost all pulmonary emboli originate in the veins of the legs, where venous pressure is lower and conditions favor clot formation. A doppler scan of the veins in my legs showed the right leg clear of clots, while my left leg showed a new clot behind my knee. An echo cardiogram showed that my right ventricular pressure was 60 mm at rest, instead of a normal 20 mm, revealing the extent to which my heart had been working to overcome the blockage in my pulmonary arteries.

Heparin

Subcutaneous injections of heparin immediately increases the activity of antithrombin III, which inhibits clotting factors Xa and IIa in the contact activation coagulation pathway formerly known as the intrinsic pathway. Factor Xa in particular is the catalyst for the conversion of prothrombin to thrombin. Inhibiting it therefore reduces thrombin which reduced fibrin formation in clots.

Warfarin

Administered orally, it gradually results in the production of undercarboxylated versions of clotting factors II, VII, IX, and X; these relatively inactive factors are collectively referred to as PIVKAs (proteins induced [by] vitamin K absence/antagonism), and individual coagulation factors as PIVKA-number (e.g. PIVKA-II). Specifically, warfarin acts by inhibits the VKORC1 subunit of vitamin K epoxide reductase, responsible for recycling vitamin K epoxide back to vitamin K and vitamin K hydroquinone.

Because it also negatively impacts the regulatory proteins C, S, and Z, it initially has the undesireable effect of increasing clotting rates, which is an added reason heparin is administered with it initially, especially when warfarin concentrations are being rapidly increased.

Prothrombin time

To gauge the correct dose of warfarin, clot-formation time is measured by exposing a blood sample is to animal tissue. INR (International Normalized Ratio) is the standard used in this measurement, endorsed by the World Health Organization. Normally, without anticoagulants, human INR measures in the 0.8 to 1.2 range. Desired range for anticoagulation therapy is 2.0 to 3.0. Specifically, what is being measured is the tissue factor coagulation pathway, formerly known as the extrinsic pathway, which is impacted by warfarin therapy.

Once the desired INR 2.0-3.0 is established, there is little danger of excessive bleeding. A study published in 2007 concluded that in 2004 in the US, there were 30 million warfarin prescriptions and 46 deaths primarily caused by anticoagulation. In the event an antidote is needed to warfarin, in order to increase coagulation rates, Vitamin K and fresh-frozen blood plasma can be administered.

Aspirin

After my bout of DVT in 2001, my internist took me off warfarin after the clots had been resorbed, and suggested a longterm low-dose (81 mg daily) aspirin regimen. I adhered to that for a few years, then stopped. Now that I have suffered a second more serious occurence with emboli, my internist is recommending longterm warfarin therapy. A condensed account of how aspirin interfers with clotting by altering platelets: thromboxane A2 is normally released by platelets to attract other platelets when physiological conditions trigger the clotting reaction; aspirin irreversibly inhibits thromboxane A2 release by inhibiting cyclooxygenase 1 (COX1); the platelets that are inhibited cannot recover normal functioning, therefore clotting will not return to normal until all or most inhibited platelets are removed from circulation and replaced by normal platelets. Other NSIDs also interfer with platelet functioning, but not irreversibly. Therefore they are not useful in longterm hypercoagulation therapy.

Risk factors for DVT and PE

Surgery, hospitalization, advanced age, obesity, infection, dehydration, immobiization, estrogen-containing contraception, tobacco use; prolonged air travel can combine dehydration and immobilization.

Cause of deaths with PE

The immediate mechanism of death is commonly suffocation or heart failure. A common misconception is that pulmonary emboli can cause stroke. The reverse is true. Clots that originate in the brain can sometimes break free and travel to the lungs, where then can result in sufficient blockage to circulation to result in death.

FAA requirements

FAA regulations and requirements related to my second class medical certificate: unless and until my lungs are clear of clots and my warfarin therapy stabilized, I will not be acting as pilot in command or other required pilot crew member, in compliance with Title 14 CFR, section 61.53, Prohibition on Operations During Medical Deficiency.

By the time of my next pilot’s medical examination, the FAA is going to need see information on family history of thrombotic disease. My father died of heart failure in 1980 at age 67, several years after being diagnosed with congestive heart disease. He had had rheumatic fever at age 13, and likely had mitral valve damage as a result. I rarely saw him in shorts, and rarer still sockless. But when I did, I remarked on the shiny red skin on one or both ankles, often with raw ulcers. It is likely these were post-thrombotic symptoms of undiagnosed DVT and/or PE.

The FAA will want to see recent tests on levels of protein S and C, which are essential components in the normal anticoagulation cycle that keeps unwanted blood clots from forming. Activated protein C (APC) in particular inactivates clotting factor Va, slowing the clotting process. If testing shows APC is not functioning normally, then the FAA will request testing for the factor V Leiden gene mutation, which is usually the cause of this abnormality. It is named after the city Leiden in The Netherlands, where it was first identified in 1994. These tests are typically performed several months after a thrombotic event such as the PE I just experienced. I will need to be taken off warfarin temporarily to allow the tests to accurately show concentrations and effectiveness of protein S and C.

Looking ahead

For the time being, I will be taking warfarin orally in sufficient doses to keep my INR in the desired 2.0-3.0 therapeutic range, checked regularly by my internist, and potentially self-tested on a device such as the InRatio2 by HemoSense. In the longer term, testing is been done on a class of drugs called direct thrombin inhibitors that promise improvement in dose-determination, monitoring, and interaction with food and other drugs. They also generally have a lower half-life than warfarin, permitting easier restoration of hemostatis when required.

One such drug, Ximelagatran, initially showed good efficacy compared with warfarin, but recently development was stopped by manufacturer AstraZeneca because of reports of liver enzyme derangements and liver failure. Dabigatran is under development for similar indications. Recent studies have indicated Dabigatran is slightly more effective than warfarin.

I will renew my lost dedication to limiting long flight legs. When necessary, I will be careful to move my legs and contract my calves regularly, getting up and moving around the cabin when practical, and drinking adequate fluids. I plan to experiment with a Texas (condom) catheter as a possible means to easier urination in a cockpit environment.

It may be advisable to do regular doppler scans of my legs to monitor for new clot formation, especially since there were no observable symptoms in my left leg this time, though a new clot had formed.

Warfarin

Heparin

Coagulation

An approach to horticulture design that focuses key principles

• Plant suitability to site to mid-Atlantic region.
• Organic and environmentally sound gardening.
• Full season interest.
• Use of variety of plants to enhance manageability and sustainability.
• Dense planting to encourage soil stability and reduce maintenance and water needs.

My Favorite Links

• Best plants for Mid-Atlantic region:Gold Medal Plants. Plants are tested for suitability and sustainability in mid-Atlantic regionPennsylvania Horticultural Society, home of famous Philadelphia Flower Show, leaders in use of horticulture as urban renewal tool: Pennsylvania Horticultural Society.
• My favorite of Northern New Jersey’s Arboretums, Frelinghuysen Arboretum, a great place to visit to look at wide variety plants, shrubs and trees well suited to Northern New Jersey: Arboretum Friends.org.

http://maplewood.blogs.nytimes.com/2009/06/16/garden-state-shaking-up-griselda/#more-11787

Thoughts and comments on controls, and opinion on good vs. bad? 
It appears that non-natives more troublesome than natives. 

Bad: 
Creeping Charlie, Glechoma hederacea. Difficult to control perennial weed European native. Competitive. 

Buttercup, Ranunculus repens L. Competitive, deplete the land of potassium, may have negative impact on surrounding plants. European native. 

Digitaria ischaemum and D. sanguinalis. Colonizes dry stressed areas. European native. 

In Between Weeds 
Dandelion, Taraxacum. Colonizes stressed areas. Not as competitive as types noted under “Bad Weed”. 

Plantain, Plantago lanceolata; Plantago major), colonizes stressed areas, an occasional late season growth in well managed lawn. 

Good Weeds 
Wild Strawberry, Fragaria vesca. Colonizes wet/dry shade areas under trees. Attracts birds. 

Wild violet, Viola rostrata. Colonizes thought out lawn, competitive in stressed areas only. Blooms in April. American native.

Our Mid Atlantic region provides ideal water and temperature conditions to support for lawns. Lawns provide a neutral, usable surface that stands in contrast to herbaceous and shrubbery boarders. Lawns like all planted surfaces consume carbon, cool the environment and support good drainage.

The problem is not lawn per se, but rather they way we maintain them and aesthetic expectations that create environment problems and degrade soil.

Our recommendations are not only sound environment stewardship, they also improve soil, which in turn reduces maintenance requirements and will save you money. Over time your lawn will crowd out most weeds and become more tolerant of drought.

• Eliminate pesticides, herbicides and non-organic fertilizer.
• Replace chemical or synthetic fertilizers with organic. Apply early spring and around Labor Day.
• Use organically sanctioned pesticides sparingly.
• Water sparingly, and when you do, soak lawn at dawn with equivalent of no less than ½ inch or rain, prior to 8:00 AM.
• Replace synthetic weed control with organic corn based weed suppressant in early spring (doubles as Nitrogen fertilzer) and fall. See http://www.hort.iastate.edu/gluten/? for more details.
• Mow lawn with mulching lawn mower (most are these days) to leave grass clippings on lawn (free fertilizer). 
• Aerate lawn in the spring.
• Mow leaves into soil in the fall.
• Get your soil tested for mineral and PH levels. Correct with organic fertilizer and/or lime as needed.  Knowing soil conditions helps to avoid mineral and fertilizer over use. Rutgers Agriculture Extension provides testing service http://njaes.rutgers.edu/soiltestinglab/
• Tolerate a few weeds. Some of them are beneficial. Beneficial weeds include wild strawberries, violets, crocus and clover.

Today I departed Bend OR in a new Columbia 400, N1134N, bound for N07 eventually, in Lincoln Park NJ, where the TKS anti-ice system is scheduled to be installed. With tailwinds forecast to be 75 knots or better, and icing airmets below 18,000 ft enroute, I chose FL250 as cruising altitude, both to take maximum advantage of the tailwind, and to stay well above clouds that might contain ice.

It worked out well. Five hours after departing at about 0945 PDT, N1134N touched down in Madison WI, (KMSN), having covered about 1400 nm on 88.5 gallons of 100LL. The wind held up at 75-85 kts on the tail, gradually diminishing and backing around from west to southwest, allowing us to average about 280 kts groundspeed. It was my demi-Demy leg. I suppose I could have stretched it for another hundred miles or so by throttling back. But my aim was different than one of Steve’s record attempts. I just wanted to get well clear of the mountains, and more than half way to my destination.

Weather was as forecast, with a broken to overcast layer below from Oregon to the Minnesota border, smooth to light turbulence, and almost exactly standard ISA temperature at FL250, -36 dC. Onboard weather data showed two quasi-stationary/cold fronts, one roughly paralleling our course to the north, the other to the south. East of the South Dakota/ Minnesota border, the undercast disappeared, replaced by a thin overcast above. That layer dissolved near Minneapolis, just before we crossed the area where the charts showed we would be expected to cross the benign cold front.

Over the Rockies, one’s thoughts turn to tactics to deal with the unlikely possibility of diverting to a high elevation alternate in response to a system problem. The topographic information provided by the Garmin G1000 MFD helps one picture the situation below, with a precise digital readout of maximum and minimum elevation within the selected range, along with a black bracket to reinforce the same data graphically on the legend, and a white horizontal line against the blue color representing the sky to show your altitude relative to the terrain below.

Performance figures, noted at two points enroute:

March 17, 2009 1720Z

MP 31.5 inches
RPM 2480
FF 16.0 gph
TIT <1615 dF
EGT <1575 dF
CHT <340 dF
OIL TEMP 171 dF
OIL PRESSURE 45 psi
TAS 210 knots
IAS 140 knots
GS 280 knots
FL250
OAT -36 dC (IAS -1 dC)

March 17, 2009 1900Z

MP 31.5
RPM 2480
FF 16.8
TIT <1625 dF
EGT <1585 dF
CHT <360 dF
OIL TEMP 176 dF
OIL PRESSURE 43 psi
TAS 218 knots
IAS 148 knots
GS 290 knots
FL250
OAT -36 dC (IAS -1 dC)

Old methods.

In 1983, when I learned to fly in an ancient C172, the only engine-related instruments were an oil pressure gauge and an oil temperature gauge. We were taught not to lean from full rich until we reached cruise, and never below 3000 ft. The method was to lean until RPM decreased, then enrichen a little. Imprecise. But given that this was a normally-aspirated engine, it was sufficient to keep us out of trouble. Besides, more precision needed to wait on improved instrumentation along with the improvements that fuel injection brought.

The turbocharged Cessna P210, N267LM, that Sape Mullender and I ferried from Schwäbisch Hall Germany to Waterloo Iowa in 2000 had an Economy Mixture Indicator (EGT) and a set of operating instructions P210 pg 1 and pg 2 designed to keep internal cylinder pressures at a safe level by keeping fuel flow sufficiently rich of peak.

With tuned injectors it became possible to ensure that all cylinders were receiving close to the same fuel-air charge. With improved instrumentation, it became practical to monitor key temperatures in each cylinder. Indirectly, that gave the pilot indications of internal cylinder pressures and enabled us to operate piston engine more efficiently by giving us the lean of peak option.

New methods.

I had been reading John Deakin’s Pelican’s Perch, but when Scott Marti first took hold of the mixture control in a Columbia 400 and pulled it back from 38 gph to 18 gph to demonstrate the big pull, I must admit I experienced an involuntary shudder. Old habits, especially in old dogs, take time to change. Now we all have flown thousands of hours using these new methods, and we know they work well. But they must be thoroughly understood if we want to use them most efficiently, and they are not reducible to a simple set of instructions.

Dr. Wayne Isom, who I frequently fly with, makes a comparison with new interns learning diagnosis. They come out of medical school with a set of useful numbers tatooed on their brains, like pO2 96% to indicate satisfactory respiration. He watched one miss a collapsed lung by focusing on that number and missing a rapid respiration rate.

More than once I have had pilots tell me they run their engines at 31.5 in MP, 2450 rpm, with FF at 18 gph. Like that 96, those are useful numbers, but not the whole story.

Future methods.

Low initial cost and low operating costs will keep piston engines in small aircraft for some time. We are likely to see changes in fuel. A company called Swift Enterprises for example, currently has a formulation called 702 in testing at the FAA William J. Hughes Technical Center at Atlantic City Airport in New Jersey. Preliminary tests showed the mixture, made from biomass, meets or exceeds the standards for 100LL avgas without any petroleum-derived components, and without lead. We are also likely to see variable timing on ignition systems with the advent of automated engine management systems such as the one called PRISM that GAMI is working on. The PRISM times the spark by directly referencing the internal cylinder pressure. We may see better designed fuel injection systems as well. Diesel engines like Thielert’s may become more widely used. They offer piston efficiency burning Jet A or road diesel fuel. Their Centurion 2.0, for example, is a turbocharged 4-stroke water-cooled 135 hp engine with a compression ratio of 18:1. Over 100 aircraft are equipped with it.

Animated model.

To focus discussion, a Flash animation has been developed, copyrighted by Principia Inc., 2009. Access is free to individuals for private use. Organizations or individuals who wish to offer the animation to the public will require a commercial license. To obtain a login, email Principia Inc.

Go to Principia client area to login and open the animation. It will persist in your browser’s cache, even without an internet connection, until you manually clear the cache or turn off your machine.

A Flash plug-in is available from Adobe if not already installed in your browser.

In the cylinder view, you will see a representation of the two flame fronts spreading out from the two spark plugs. Of course, that is an idealization. To see an actual video taken inside an operating cylinder, go here on YouTube.

Five red buttons on top control (from left) page, either panel or cylinder; pause crankshaft rotation; step one frame; zoom; select individual frames.

Three gauges and four sliders are active controls: MP, RPM, FF, SPARK, IAS, OAT, and OCTANE.

Fuel flow (FF) can be set independently by clicking on the FF pointer and moving it to the desired level.

Seven graphs display results of changes in variables, from top left, turbine inlet temperature (TIT), exhaust gas temperature (EGT), cylinder head temperature (CHT), internal cylinder pressure (ICP), brake horsepower (HP), air to fuel ratio (A:F), and brake specific fuel consumption (inverted), a measure of fuel efficiency (1/BSFC); colors are used to depict temperature changes, ranging from yellow (cooler) to red (hotter); colors are used to indicate air/fuel ratio ranging from light blue (leaner) to dark blue (richer); redlines on TIT and CHT are indicated.

Failures are selected with toggle keys along the bottom: INJECT/VAPOR for effect of reduced fuel flow from either plugged injector or vapor lock; PLUG for one failed spark plug; CHT-IND for a failed CHT probe; DETON for detonation; PREIGN for preignition; VALVE for an exhaust valve stuck partially open; and CRACK for a crack in the exhaust manifold

Variations.

MP (throttle) increase results in higher potential internal cylinder pressures as indicated indirectly by TIT, EGT, and CHT data.

RPM (engine and prop revolutions) increase tends to increase fuel flow due to increase in engine-driven fuel pump speed.

FF (fuel flow) adjust to show impact of air:fuel mixture changes.

Spark timing can be advanced or retarded to illustrate the impact of earlier or later ignition.

OAT (outside air temperature) increase tends to cause internal cylinder pressures (ICP) to rise by decreasing air-cooling efficiency; also tend to limit maximum LOP fuel flow by limiting available oxygen mass in the mixture.

IAS (indicated air speed) increase tends to decrease ICP by improving air-cooling efficiency.

Octane increase decreases the rate of flame front progress.

Examples.

Hot and high cruise: MP 32 IN RPM 2500 IAS 150 OAT -5 C (ISA +30 at FL250).

Already only about half as dense at this altitude, cooling air is also warmer than standard. Result is less efficient cooling, resulting in higher pressures and temperatures in the combustion chamber, reflected in higher TIT, EGT, and CHT indications. Induction air, being warmer, is less dense than standard, even after being compressed by turbochargers. It therefore contains fewer oxygen molecules, and is able to oxidize fewer fuel molecules. In light of those two factors, LOP fuel flow will need to be lower than standard to keep cylinder pressure (as indirectly indicated by TIT, EGT and CHT) at an acceptable level.

Cessna’s PIM for the 400, RC0500005HIM, Revision level H, pg 5-32, suggests a fuel flow of 15 gph might work under these extremely hot conditions, to keep TIT at a value at least 50 dF below peak. It might. But rather than setting that fuel flow, and accepting whatever TIT results, the prudent pilot will reduce fuel flow until TIT cools to 1625 dF or below, and monitor CHTs to ensure they do not rise much above 380 dF. More prudent still to set fuel flow to keep CHTs below 380, even though it might mean sacrificing airspeed. Suppose that 15 gph turns out to work. The 7.5:1 compression ratio in for the TSIO-550-C produces 13.7 BHP per gph LOP, yielding 205 of 310 maximum, or about 66%.

That same page in the same PIM predicts 231 KTAS under these same conditions, which yields 147 KIAS. Interestingly, that airspeed prediction is marginally better than what is predicted at standard conditions, despite the predicted lower fuel flow and lower BHP. What gives? Less dense air at warmer than standard temperatures has one nice positive outcome: higher airspeed due to lower parasitic drag.

Autogas: hypothetical but educational. Substituting regular US auto fuel for 100LL avgas.

FAA-approved STCs are available for most lower compression aircraft engine installations, but no turbocharged engines and not for Part 135.

Why just lower compression engines? The lower octane rating of auto fuels signifies among other characteristics, their lower auto-ignition temperatures. That is the temperature (pressure) at which a gaseous fuel mixed with air will supply the energy to support combustion. In a diesel engine, we want a relatively low auto-ignition temperature. That is because a spark plug is not used to trigger ignition. Instead, liquid fuel is injected directly into the cylinder once the piston is starting down after compressing air in the combustion chamber and thereby raised the temperature above diesel fuel’s auto-ignition temperature by compression. The injected diesel fuel immediately vaporizes and combusts, creating additional heat and pressure to accelerate the piston down.

However, in engines designed to burn avgas or autogas, a mixture of fuel vapor and air is pulled into the combustion chamber on an intake stroke, then compressed on the next stroke, during which process, it must resist the urge to spontaneously combust before ignited by the spark plug at the end of the compression process. Otherwise, the cylinder could be damaged. This is known as pre-ignition. For 100LL avgas, that auto-ignition temperature is about 440 dC. For auto fuels, it is much lower, about 260 dC. Hence the limitation to lower-compression aircraft engines.