If you are an adult and you fly an airplane, there is a decentchance that you will develop hypertension during your flying lifetime. Some 20 percent ofadult Americans are afflicted by this symptomless malady, which has been aptly termed the”silent killer.” Certainly you have a better chance of becoming hypertensivethan you do of flying your aircraft into terrain. However, the outcome of both of theseevents can be the same: sudden death. That’s why it’s absolutely essential for everyairman to take the steps necessary to diagnose and treat the disease.
My purpose in writing this article is to explain how the body regulates blood pressure,how those mechanisms can go awry, how hypertension can lead to grief, and how it iscommonly treated. We’ll also deal with the FAA’s stance on hypertension with respect tomedical certification of pilots. By the time we’re through, I hope to convince you that ifyou have hypertension, you must treat it properly — and that with proper treatment, youshould have no problems qualifying for an FAA medical certificate and continue flying.
Quick Tour Of The Human Circulatory System
Essentially, the human circulatory system is a closed-loop, recirculating pumpingsystem. Its job is to deliver oxygen and nutrients to body tissues for their use, and toretrieve and transport carbon dioxide and other waste products from those cells back tothe organs — mainly liver, kidneys, and lungs — where they are detoxified or eliminated.Its function is mostly, therefore, logistics and transportation.
The system consists of a double pump, the heart; plumbing leading away from theheart on the high-pressure, or arterial, limb of the system; and plumbingleading back to the heart on the low-pressure, or venous limb. Interposed betweenand connecting the arterial and venous limbs of the system, more or less in a parallelarrangement, are millions of highly permeable tubes called capillaries, containedwithin organs and tissues. These microscopic channels — some so narrow that redblood cells must transit them in single file — are the site of nutrient and waste productexchange. (I described such a capillary system within the lung in my previous AVwebarticle, “How Does Oxygen Work?“)
To help illustrate the overall flow of the system, let’s follow the journey made by asingle red blood cell. Red blood cells are the “trucks” that actually hold thehemoglobin molecules which carry oxygen to the tissues. They have a life span of three orfour months, during which they make countless trips around the circulatory system and willultimately wind up visiting most or all of the body’s organs. But for the moment, let’ssuppose the particular red blood cell we’re watching is destined for the kidney.
Our red cell, suspended in the liquid blood plasma, leaves the left side of theheart via the aorta, the major artery of the body which runs down the back of yourchest and abdominal cavities near your spine. Next, this cell leaves the aorta to enterthe renal artery, the major “feeder” artery for the kidney. Once withinthe kidney itself, our cell flows through a series of arteries of gradually decreasingdiameter, feeding next into an arteriole (very small artery). Finally, ourperipatetic corpuscle flows from this arteriole into a capillary bed where it givesup its oxygen to the kidney’s tissues and takes on its load of wastes from those tissues.
Exiting the capillary bed, our now-deoxygenated red cell enters the low-pressure venousloop of the system. It travels into a venule (very small vein); thenthrough a series of veins of gradually increasing size within the kidney; then into the renalvein (the major “draining” vein for the kidney); and then into the venacava (the major return route for blood from the lower half of the body). Finally, itarrives back at the heart — the right side this time. From there, it makes a quick tripthrough the pulmonary system (lungs) to dump its carbon dioxide and reload withoxygen, whereupon it returns to the left side of the heart where the journey begins again.
A further word about arterioles and venules. These tiny blood vessels are importantregulators of blood flow and pressure. They stand like sentinels at each end of acapillary bed, where by varying their diameters, they can regulate flow into and out ofthe capillary beds they serve. We’ll see in a moment how varying diameter, and thusresistance, can affect blood flow.
This system has a complex set of regulatory mechanisms, most of which work via”negative feedback” loops. These regulatory mechanisms, largely theresponsibility of your autonomic nervous system, tend to maintain your bloodpressure at or near your body’s “set point,” blunting deviations from this setpoint whether higher or lower. A rise in blood pressure away from the set point, forinstance, is met with a negative or inhibitory response which tends to lower the pressureback towards normal. One of the problems with hypertension, as we’ll further explorelater, is that this “set point” is askance; it is higher than in nonhypertensivepatients.
What Determines Blood Pressure?
We have to consider some of the flow dynamics of the system in order to understandthese concepts better. I have found it helpful to liken the whole system to a network ofpumps and pipes whose job it is to circulate a fluid. To apply the example of ourtheoretical pump-and-pipe circulatory system, we must make certain assumptions which aredifferent from the actual human situation: that the pipes are rigid and inelastic, unlikehealthy, muscular, flexible blood vessels; and that the fluid has low viscosity, unlikehighly viscous, cell-filled blood.
I know we all remember Ohm’s Law, which describes the relationship between current (I),voltage (E), and resistance (R) in an electrical circuit:
I = E / R
This formula makes it clear that electrical current changes in the same direction asdoes the voltage across a circuit , but is inversely proportional to the resistance ofthat circuit. More voltage or less resistance means more current; less voltage or moreresistance means less current.
The same principles apply in fluid systems such as the human circulatory system. Here, flowQ replaces current; and pressure P replaces voltage. Resistance Rremains as before. So we have:
Q = P / R
We will increase flow if we increase the pressure gradient across a capillary bed ordecrease its resistance; and we will decrease flow by lowering the pressure gradient or byincreasing the bed’s resistance. Keep in mind that resistance in a fluid system isproportional to the length of the “pipe” and varies inversely to the diameter ofthe pipe.
Adapting our nomenclature to the circulatory system, we get the following:
CO = BP / SVR
Where CO is Cardiac Output, a measure of flow; BP is (three guesses!) BloodPressure; and SVR is Systemic Vascular Resistance, a composite of all the resistances ofall the blood vessels in the body, most of which behave as if they are arranged inparallel.
Rearranging this equation to solve for blood pressure, we get:
BP = CO x SVR
Cardiac output is the volume of blood the heart can pump in a given amount oftime, usually expressed in liters per minute (L/min). Cardiac output is affected by anumber of factors, and can be expressed as the product of heart rate (HR) measured in”beats per minute” and stroke volume (SV), the volume of blood pumped with eachbeat:
CO = HR x SV
If you combine the last two equations by substitution, you see that blood pressure is afunction of three variables:
BP = HR x SV x SVR
Stroke volume depends on how full the whole system is and how efficiently the heartmuscle cells are contracting and squeezing the blood out of the heart. For instance, heartmuscle cells damaged by a previous heart attack might cause the heart to pump less bloodwith each beat than a healthy heart. To maintain a normal cardiac output with a diminishedstroke volume (SV), the heart must compensate by beating faster (higher HR). Of course,there might come a point where so much heart muscle is damaged that these compensatorymechanisms can no longer compensate for the decline in stroke volume. If this situationleads to a cardiac output inadequate for the body’s needs, then heart failure isthe result.
Let us add some numbers to help all of this make sense. If you are a fit adult maleyour stroke volume might be 100 milliliters (mL) and your heart rate might be 65 beats perminute. In one minute your heart will pump 65 times 100, or 6500 mL. Move the decimalplace around a bit and you get a cardiac output of 6.5 L/min. You’re doing well. In fact,many well-trained athletes have astonishing cardiac outputs, along with low heart rates(sometimes in the 40s or 50s!), indicating a large stroke volume and a very efficientcirculatory system.
To keep things simple, we will assume for most of this discussion that cardiac outputremains constant as blood pressure, resistance, and/or heart rate vary. This is not alwaysthe case in real life, but we don’t want to make things too messy for our purposes here.
BP Regulation and Hypertension
Blood pressure regulation is a complex and elegant symphony, but one which can go awryin any of a number of ways. Fortunately for our discussion, most hypertension is caused bya problem of vascular resistance, of stroke volume/cardiac output, or a combination ofboth of these. And equally fortunately, specific treatments have been devised to attackthese specific kinds of trouble, as we’ll see shortly.
You are probably aware that a person’s blood pressure measurement consists of two numbers, the “top” or systolic, and the “bottom” or diastolic, pressures. These numbers respectively reflect the pressure in the system during a heartbeat when blood is being forcefully ejected from the heart, and the pressure during the time between beats when the heart is briefly at rest, filling up for the next beat. Each of these numbers has separate significance for diagnosis and treatment.
For instance, in male patients with only diastolic hypertension, treatment to lower blood pressure has been demonstrated to reduce death and complication rates from cardiovascular disease. On the other hand, although male patients with systolic hypertension but normal diastolic pressures suffer twice the cardiovascular-disease death rate of their normotensive fellows, for this group a treatment-induced reduction in these death rates has not been definitively demonstrated. It is for this reason that many practitioners may be more willing to tolerate mild to moderate elevations of systolic pressures than of diastolic pressures, all other things being equal, in a person who has no other risk factors for cardiovascular disease.
Although controversy has raged over exactly what pressure readings constitute a”normal” blood pressure, we usually say that a systolic reading ofgreater than 140 millimeters of mercury (mm Hg), or a diastolic reading of greaterthan 90 mm Hg, is abnormally high. These “normal” numbers rise a bit with age sothat a blood pressure of 150/ 94 might be considered acceptable in a 70 year old.
The decision whether to treat an elevated blood pressure depends on the degree ofelevation of one or both numbers, and on a consideration of the patient’s total medicalpicture and the presence of other risk factors for cardiovascular disease such as smoking,obesity, family history, and diabetes. An otherwise healthy patient with mild hypertensionmight be prescribed only exercise, salt and fat moderation, and regular observation.
The diagnosis of hypertension should be based on more than one reading of bloodpressure taken on more than one occasion under calm, controlled conditions. The anxietymany of us feel when having our blood pressure taken — especially when our recreation orlivelihood may hinge on the outcome — can produce a transient rise in blood pressure thatdoes not indicate chronic hypertension. This “white coat hypertension” can bediscovered by multiple careful readings after the patient has had time to relax for awhile before each reading. Alternatively, some patients wear a portable device thatmeasures blood pressure periodically over 24 hours, giving a profile of the patient’sblood pressure during normal daily activities.
Hypertension is classified by its probable causation as primary (essential) or secondary.Secondary causes make up only ten to fifteen percent of cases of hypertension in thiscountry and are more common in younger females than in males. In cases of secondaryhypertension, there is an identifiable and often correctable underlying problem, such as anarrowing of the artery to a kidney or an overproduction of certain blood-pressure-raisinghormones. Typically, once the cause is identified and corrected, the hypertension goesaway with no further need for treatment. Primary hypertension, on the other hand,constitutes the vast majority of cases of hypertension. It does not have a singlerecognizable cause and usually requires lifelong, daily intervention to keep bloodpressure under control.
Primary hypertension is thought to result from defects in the mechanisms that regulateblood pressure in one or more of several areas. For instance, there can be an abnormalityin the body’s regulation of salt and water balance, resulting in “overfilling”of the vascular system so that the whole system is “overpressurized” — theheart must pump a higher flow against a constant resistance, raising the pressure of thesystem. Or, there may exist an abnormality in the regulation of vascular resistance by theblood vessels of the body, especially arterioles, such that system resistance isabnormally high — in this situation, the heart pumps a normal flow against a higherresistance, raising blood pressure. Alternatively, the heart may pump a normal flow, butwith an excessive contractile force, against a normal resistance, again raising thepressure within the system. These various mechanisms may act singly or in combination, andas we begin treatment we do not always know exactly which error predominates in a givenpatient. For this reason, especially early in the course of treatment, varying dosagesand/or drug combinations must often be tried before the right regimen is found for a givenpatient.
Why Is Hypertension So Dangerous?
Untreated, hypertension can lead to serious health consequences, including death. Ofcourse, death disqualifies you for the issuance of a medical certificate. In fact, yourAME is authorized to make this determination without calling Oklahoma City.
Equally damaging to your flying career are some of the other complications ofhypertension we’ll discuss in a moment.
How quickly one comes to grief from hypertension depends on the duration of thehypertension, its severity, and the presence or absence of other cardiovascular riskfactors. Very severe (acute) hypertension for a short time can cause problems, as can lesssevere hypertension over a period of many years (chronic). We will focus on the lattersituation — chronic essential hypertension — since it represents the norm for mostpatients.
Hypertension harms and kills because it damages the blood vessels of certain vitalorgans, most often the heart, brain, and kidneys. Heart attack, heart failure, stroke, andkidney failure are the most common manifestations of this blood vessel damage inhypertensive patients. The final common mechanism of these maladies is decreased bloodflow, or perfusion, to those organs through blood vessels damaged by yearsof hypertension. Along with diabetes, smoking, elevated blood cholesterol, family history,and obesity, hypertension is a major risk factor for cardiovascular disease.
Arterioles subjected to the increased force of an elevated blood pressure respond bythickening. These arterioles are “programmed” not to allow a large increase inflow through the capillary beds they guard, so they must constrict to increase theirresistance to keep flow through those beds constant. Over many years, the walls of thesevessels may actually thicken inward so much that blood flow through them is dangerouslyreduced. The capillary beds downstream from these arterioles receive an inadequate bloodflow, causing damage to the cells, tissues and organs those capillaries serve.
Additionally, hypertension alone or in concert with the other risk factors above candamage larger blood vessels such as the carotid arteries of the neck that provideblood to the brain, or the coronary arteries supplying blood to the heart muscle.In this situation, injured blood vessel linings accumulate plaques of cholesteroland other nasty stuff which — like sludge in a pipe — can narrow the channel within thevessel so much that blood flow is significantly reduced. If this happens over a longperiod of time, alternate channels of blood flow called collaterals may develop toact as alternate supply routes for the hungry tissues beyond those blockages.
However, what often happens is that a plaque within one of those arterial wallsruptures, exposing its rough and shaggy interior to the blood passing over it in theartery. The ragged surface of this ruptured plaque is a powerful stimulus to bloodclotting. The resulting clot over the ruptured plaque may completely occlude the artery.If collateral circulation is not adequate to meet the needs of the tissue beyond theblockage, that tissue begins to die of oxygen and nutrient starvation. When this happensin the heart, one suffers a myocardial infarction, or “heart attack.”
A similar process can happen to the brain. Here, the culprit is usually a plaque in oneof the carotid arteries in the neck. This shaggy plaque develops clots on its surface,which may fragment and travel downstream into the brain until they wedge in a smallartery, blocking it completely and causing brain cells to die. The result is called a stroke.The problem here is that — like the heart muscle — the brain has poor collateralcirculation. A given brain cell might get its blood from a single small blood vessel.Occlude that vessel, and its dependent cells starve and die.
Years of high blood pressure are tough on the heart in other ways besides throughblockages of the coronary arteries. The heart muscle has to work hard to pump its bloodout against an elevated pressure. The heart muscle thickens in an effort to accomplishthis increased work load more efficiently. If the heart muscle gets thick enough it maylose flexibility — like an overly bulked-up body builder — and not be able to relaxsufficiently to allow the heart’s pumping chambers to fill between beats, causing heartfailure. Also, thickened heart muscle requires quite a bit more oxygen to do its work,and is therefore more susceptible to any interruption of the supply of oxygen-rich bloodto the heart muscle itself. All things being equal, a thickened, stiff heart can toleratereductions or interruptions in its coronary blood flow much less well than a normal,healthy heart.
As our understanding of the various mechanisms of hypertension has improved, logicalavenues for its treatment have been developed. For instance, hypertension caused byexcessive salt and water retention in the circulatory system can be treated by a low-saltdiet, or with diuretic drugs that cause the kidneys to shed the excess salt andwater, restoring a normal blood volume. Hypertension due to elevated resistance orexcessive contractile force of the heart often responds to drugs that decrease vascularresistance by relaxing arterioles (e.g., ACE inhibitors) or decrease the force ofcardiac contraction (e.g., beta blockers).
For an individual patient, it cannot usually be determined up front which of theseprecise mechanisms is at fault. However, certain groups of patients seem to respond betterto one type of drug or another, suggesting that the mechanisms have a certain geneticpredisposition. For instance, African-American hypertensives as a group seem more likelyto respond to drugs which attack salt retention or vascular resistance, rather than todrugs which decrease cardiac contraction force, suggesting that volume overload orelevated vascular resistance may be more often the cause of their hypertension than forother groups. There are demographic differences noted for other groups as well, such asthe elderly and for middle-aged white males.
The usual treatment strategy is first to try non-medication strategies such as weightloss, exercise, and salt restriction. If these do not produce the desired decrease inblood pressure, the usual next step is to begin with a single antihypertensive medicationat low dose. The type of drug is chosen based on considerations of age, sex, race, andother medical problems the patient might have. The dose of this drug is graduallyincreased until its maximum dose is reached, until side effects limit further increases,or (we hope) until the desired decrease in blood pressure is attained. If this procedurefails for one drug, then another is chosen and the process begins again. Or, a second drugmay be added to the first. Using a combination of two drugs to treat hypertension is oftenadvantageous, since using drugs with complementary properties may allow a lower dose ofeach drug than if either was taken alone. Since side effects are often dose-dependent,this is good news. For the majority of hypertensive patients, good blood pressure controlcan be maintained on one or two drugs, often taken only once per day. (Most newerhypertension drugs are designed for once- or twice-per-day dosing at most.)
I have summarized the major categories of antihypertensive drugs and their actions andside effects in the following table:
|Drug Category||Examples||Major Mechanism
or Site of Action
|Most Likely Potential
|Salt and water retention||Low blood potassium
Dizziness on standing
Abnormal blood cholesterol
|Cardiac contraction strength||Fatigue
Shortness of breath
Dizziness on standing
Interference with diabetic treatment
|Calcium Channel Blockers||Procardia Cardizem
|Cardiac contraction strength
Shortness of breath
Swelling of feet/hands
Decreased kidney function (blood test)
High blood potassium
|Vascular resistance||Dizziness on standing|
|Vascular resistance||Dizziness on standing
The FAA and Hypertension
Gone are the days in which a diagnosis of hypertension meant the end of one’s flyingcareer. This welcome change in regulations and attitudes in Oklahoma City has paralleledthe vast improvement in understanding, diagnosis, and treatment of the disorder.
In simplest form, the regulations state that if you have sustained and multiple bloodpressure readings of greater than 155/95 you must have a medical evaluation and begin atreatment program. The medical evaluation is designed to demonstrate that you have notsuffered any significant complications from hypertension, such as described in thisarticle, that might make unsafe the operation of an aircraft.
Once your blood pressure returns to the normal range and you have demonstrated noadverse effects from the medications, you can receive a medical certificate. Your treatingphysician will need to supply your AME with several items of information about yourevaluation and treatment. This usually includes an EKG and sometimes a blood workup.Provided that the information reveals good blood pressure control with acceptable sideeffects and no evidence of organ damage from hypertension, your AME can issue your normalcertificate. This information is summarized at
It would be a good idea to bring a list of FAA-approved antihypertensive medications with you when you visit your doctor, especially if he or she is not also an AME. In this way you can have a “custom designed” treatment regimen which will raise no red flags with the FAA. This list was previously available online at the Civil Aeromedical Institute (CAMI) website, , but the link is now defunct. In general, beta blockers, calcium channel blockers, ACE inhibitors, and diuretics will pass FAA muster, while sympatholytics and alpha blockers might raise eyebrows due to potential central nervous system side effects. You should ask your own AME to give you more specific information about approved medications prior to consulting your treating physician.
I hope by now you are convinced of the absolute necessity of proper treatment ofhypertension, and that you now have a basic understanding of what can go wrong and how itcan be fixed. Remember that, armed with information and a determination to adhere to thetreatment plan your physician has outlined, you can keep on flying with hypertension, nowand for many years to come.