May 13, 1999 Blood Pressure Basics For Pilots

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by	Michael D. Sebastian, M.D.
	Contributor

If you are an adult and you fly an airplane, there is a decent chance that you will develop hypertension during your flying lifetime. Some 20 percent of adult Americans are afflicted by this symptomless malady, which has been aptly termed the "silent killer." Certainly you have a better chance of becoming hypertensive than you do of flying your aircraft into terrain. However, the outcome of both of these events can be the same: sudden death. That's why it's absolutely essential for every airman 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 is commonly treated. We'll also deal with the FAA's stance on hypertension with respect to medical certification of pilots. By the time we're through, I hope to convince you that if you have hypertension, you must treat it properly -- and that with proper treatment, you should 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 pumping system. Its job is to deliver oxygen and nutrients to body tissues for their use, and to retrieve and transport carbon dioxide and other waste products from those cells back to the 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 the heart on the high-pressure, or arterial, limb of the system; and plumbing leading back to the heart on the low-pressure, or venous limb. Interposed between and connecting the arterial and venous limbs of the system, more or less in a parallel arrangement, are millions of highly permeable tubes called capillaries, contained within organs and tissues. These microscopic channels -- some so narrow that red blood cells must transit them in single file -- are the site of nutrient and waste product exchange. (I described such a capillary system within the lung in my previous AVweb article, "How Does Oxygen Work?")

To help illustrate the overall flow of the system, let's follow the journey made by a single red blood cell. Red blood cells are the "trucks" that actually hold the hemoglobin molecules which carry oxygen to the tissues. They have a life span of three or four months, during which they make countless trips around the circulatory system and will ultimately wind up visiting most or all of the body's organs. But for the moment, let's suppose 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 the heart via the aorta, the major artery of the body which runs down the back of your chest and abdominal cavities near your spine. Next, this cell leaves the aorta to enter the renal artery, the major "feeder" artery for the kidney. Once within the kidney itself, our cell flows through a series of arteries of gradually decreasing diameter, feeding next into an arteriole (very small artery). Finally, our peripatetic corpuscle flows from this arteriole into a capillary bed where it gives up 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 venous loop of the system. It travels into a venule (very small vein); then through a series of veins of gradually increasing size within the kidney; then into the renal vein (the major "draining" vein for the kidney); and then into the vena cava (the major return route for blood from the lower half of the body). Finally, it arrives back at the heart -- the right side this time. From there, it makes a quick trip through the pulmonary system (lungs) to dump its carbon dioxide and reload with oxygen, 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 important regulators of blood flow and pressure. They stand like sentinels at each end of a capillary bed, where by varying their diameters, they can regulate flow into and out of the capillary beds they serve. We'll see in a moment how varying diameter, and thus resistance, 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 the responsibility of your autonomic nervous system, tend to maintain your blood pressure at or near your body's "set point," blunting deviations from this set point whether higher or lower. A rise in blood pressure away from the set point, for instance, is met with a negative or inhibitory response which tends to lower the pressure back towards normal. One of the problems with hypertension, as we'll further explore later, is that this "set point" is askance; it is higher than in nonhypertensive patients.

What Determines Blood Pressure?

We have to consider some of the flow dynamics of the system in order to understand these concepts better. I have found it helpful to liken the whole system to a network of pumps and pipes whose job it is to circulate a fluid. To apply the example of our theoretical pump-and-pipe circulatory system, we must make certain assumptions which are different from the actual human situation: that the pipes are rigid and inelastic, unlike healthy, muscular, flexible blood vessels; and that the fluid has low viscosity, unlike highly 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:

This formula makes it clear that electrical current changes in the same direction as does the voltage across a circuit , but is inversely proportional to the resistance of that circuit. More voltage or less resistance means more current; less voltage or more resistance means less current.

The same principles apply in fluid systems such as the human circulatory system. Here, flow Q replaces current; and pressure P replaces voltage. Resistance R remains as before. So we have:

We will increase flow if we increase the pressure gradient across a capillary bed or decrease its resistance; and we will decrease flow by lowering the pressure gradient or by increasing the bed's resistance. Keep in mind that resistance in a fluid system is proportional to the length of the "pipe" and varies inversely to the diameter of the pipe.

Adapting our nomenclature to the circulatory system, we get the following:

Where CO is Cardiac Output, a measure of flow; BP is (three guesses!) Blood Pressure; and SVR is Systemic Vascular Resistance, a composite of all the resistances of all the blood vessels in the body, most of which behave as if they are arranged in parallel.

Rearranging this equation to solve for blood pressure, we get:

Cardiac output is the volume of blood the heart can pump in a given amount of time, usually expressed in liters per minute (L/min). Cardiac output is affected by a number 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 each beat:

If you combine the last two equations by substitution, you see that blood pressure is a function of three variables:

Stroke volume depends on how full the whole system is and how efficiently the heart muscle cells are contracting and squeezing the blood out of the heart. For instance, heart muscle cells damaged by a previous heart attack might cause the heart to pump less blood with each beat than a healthy heart. To maintain a normal cardiac output with a diminished stroke 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 compensatory mechanisms can no longer compensate for the decline in stroke volume. If this situation leads to a cardiac output inadequate for the body's needs, then heart failure is the result.

Let us add some numbers to help all of this make sense. If you are a fit adult male your stroke volume might be 100 milliliters (mL) and your heart rate might be 65 beats per minute. In one minute your heart will pump 65 times 100, or 6500 mL. Move the decimal place 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 efficient circulatory system.

To keep things simple, we will assume for most of this discussion that cardiac output remains constant as blood pressure, resistance, and/or heart rate vary. This is not always the 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 awry in any of a number of ways. Fortunately for our discussion, most hypertension is caused by a problem of vascular resistance, of stroke volume/cardiac output, or a combination of both of these. And equally fortunately, specific treatments have been devised to attack these 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 of greater than 140 millimeters of mercury (mm Hg), or a diastolic reading of greater than 90 mm Hg, is abnormally high. These "normal" numbers rise a bit with age so that 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 of elevation of one or both numbers, and on a consideration of the patient's total medical picture and the presence of other risk factors for cardiovascular disease such as smoking, obesity, family history, and diabetes. An otherwise healthy patient with mild hypertension might be prescribed only exercise, salt and fat moderation, and regular observation.

The diagnosis of hypertension should be based on more than one reading of blood pressure taken on more than one occasion under calm, controlled conditions. The anxiety many of us feel when having our blood pressure taken -- especially when our recreation or livelihood may hinge on the outcome -- can produce a transient rise in blood pressure that does not indicate chronic hypertension. This "white coat hypertension" can be discovered by multiple careful readings after the patient has had time to relax for a while before each reading. Alternatively, some patients wear a portable device that measures blood pressure periodically over 24 hours, giving a profile of the patient's blood 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 this country and are more common in younger females than in males. In cases of secondary hypertension, there is an identifiable and often correctable underlying problem, such as a narrowing of the artery to a kidney or an overproduction of certain blood-pressure-raising hormones. Typically, once the cause is identified and corrected, the hypertension goes away 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 single recognizable cause and usually requires lifelong, daily intervention to keep blood pressure under control.

Primary hypertension is thought to result from defects in the mechanisms that regulate blood pressure in one or more of several areas. For instance, there can be an abnormality in the body's regulation of salt and water balance, resulting in "overfilling" of the vascular system so that the whole system is "overpressurized" -- the heart must pump a higher flow against a constant resistance, raising the pressure of the system. Or, there may exist an abnormality in the regulation of vascular resistance by the blood vessels of the body, especially arterioles, such that system resistance is abnormally high -- in this situation, the heart pumps a normal flow against a higher resistance, raising blood pressure. Alternatively, the heart may pump a normal flow, but with an excessive contractile force, against a normal resistance, again raising the pressure within the system. These various mechanisms may act singly or in combination, and as we begin treatment we do not always know exactly which error predominates in a given patient. For this reason, especially early in the course of treatment, varying dosages and/or drug combinations must often be tried before the right regimen is found for a given patient.

Why Is Hypertension So Dangerous?

Untreated, hypertension can lead to serious health consequences, including death. Of course, death disqualifies you for the issuance of a medical certificate. In fact, your AME is authorized to make this determination without calling Oklahoma City.

Equally damaging to your flying career are some of the other complications of hypertension we'll discuss in a moment.

How quickly one comes to grief from hypertension depends on the duration of the hypertension, its severity, and the presence or absence of other cardiovascular risk factors. Very severe (acute) hypertension for a short time can cause problems, as can less severe hypertension over a period of many years (chronic). We will focus on the latter situation -- chronic essential hypertension -- since it represents the norm for most patients.

Hypertension harms and kills because it damages the blood vessels of certain vital organs, most often the heart, brain, and kidneys. Heart attack, heart failure, stroke, and kidney failure are the most common manifestations of this blood vessel damage in hypertensive patients. The final common mechanism of these maladies is decreased blood flow, or perfusion, to those organs through blood vessels damaged by years of 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 by thickening. These arterioles are "programmed" not to allow a large increase in flow through the capillary beds they guard, so they must constrict to increase their resistance to keep flow through those beds constant. Over many years, the walls of these vessels may actually thicken inward so much that blood flow through them is dangerously reduced. The capillary beds downstream from these arterioles receive an inadequate blood flow, causing damage to the cells, tissues and organs those capillaries serve.

Additionally, hypertension alone or in concert with the other risk factors above can damage larger blood vessels such as the carotid arteries of the neck that provide blood to the brain, or the coronary arteries supplying blood to the heart muscle. In this situation, injured blood vessel linings accumulate plaques of cholesterol and other nasty stuff which -- like sludge in a pipe -- can narrow the channel within the vessel so much that blood flow is significantly reduced. If this happens over a long period of time, alternate channels of blood flow called collaterals may develop to act as alternate supply routes for the hungry tissues beyond those blockages.

However, what often happens is that a plaque within one of those arterial walls ruptures, exposing its rough and shaggy interior to the blood passing over it in the artery. The ragged surface of this ruptured plaque is a powerful stimulus to blood clotting. 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 the blockage, that tissue begins to die of oxygen and nutrient starvation. When this happens in 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 one of 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 small artery, 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 collateral circulation. 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 through blockages of the coronary arteries. The heart muscle has to work hard to pump its blood out against an elevated pressure. The heart muscle thickens in an effort to accomplish this increased work load more efficiently. If the heart muscle gets thick enough it may lose flexibility -- like an overly bulked-up body builder -- and not be able to relax sufficiently to allow the heart's pumping chambers to fill between beats, causing heart failure. 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 blood to the heart muscle itself. All things being equal, a thickened, stiff heart can tolerate reductions or interruptions in its coronary blood flow much less well than a normal, healthy heart.

 Treating Hypertension

As our understanding of the various mechanisms of hypertension has improved, logical avenues for its treatment have been developed. For instance, hypertension caused by excessive salt and water retention in the circulatory system can be treated by a low-salt diet, or with diuretic drugs that cause the kidneys to shed the excess salt and water, restoring a normal blood volume. Hypertension due to elevated resistance or excessive contractile force of the heart often responds to drugs that decrease vascular resistance by relaxing arterioles (e.g., ACE inhibitors) or decrease the force of cardiac contraction (e.g., beta blockers).

For an individual patient, it cannot usually be determined up front which of these precise mechanisms is at fault. However, certain groups of patients seem to respond better to one type of drug or another, suggesting that the mechanisms have a certain genetic predisposition. For instance, African-American hypertensives as a group seem more likely to respond to drugs which attack salt retention or vascular resistance, rather than to drugs which decrease cardiac contraction force, suggesting that volume overload or elevated vascular resistance may be more often the cause of their hypertension than for other groups. There are demographic differences noted for other groups as well, such as the elderly and for middle-aged white males.

The usual treatment strategy is first to try non-medication strategies such as weight loss, exercise, and salt restriction. If these do not produce the desired decrease in blood pressure, the usual next step is to begin with a single antihypertensive medication at low dose. The type of drug is chosen based on considerations of age, sex, race, and other medical problems the patient might have. The dose of this drug is gradually increased 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 procedure fails for one drug, then another is chosen and the process begins again. Or, a second drug may be added to the first. Using a combination of two drugs to treat hypertension is often advantageous, since using drugs with complementary properties may allow a lower dose of each 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 control can be maintained on one or two drugs, often taken only once per day. (Most newer hypertension drugs are designed for once- or twice-per-day dosing at most.)

I have summarized the major categories of antihypertensive drugs and their actions and side effects in the following table:

 The FAA and Hypertension

Gone are the days in which a diagnosis of hypertension meant the end of one's flying career. This welcome change in regulations and attitudes in Oklahoma City has paralleled the vast improvement in understanding, diagnosis, and treatment of the disorder.

In simplest form, the regulations state that if you have sustained and multiple blood pressure readings of greater than 155/95 you must have a medical evaluation and begin a treatment program. The medical evaluation is designed to demonstrate that you have not suffered any significant complications from hypertension, such as described in this article, that might make unsafe the operation of an aircraft.

Once your blood pressure returns to the normal range and you have demonstrated no adverse effects from the medications, you can receive a medical certificate. Your treating physician will need to supply your AME with several items of information about your evaluation and treatment. This usually includes an EKG and sometimes a blood workup. Provided that the information reveals good blood pressure control with acceptable side effects and no evidence of organ damage from hypertension, your AME can issue your normal certificate. This information is summarized at http://www.cami.jccbi.gov/aam-300/bpinfo.html.

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 of hypertension, and that you now have a basic understanding of what can go wrong and how it can be fixed. Remember that, armed with information and a determination to adhere to the treatment plan your physician has outlined, you can keep on flying with hypertension, now and for many years to come.