- Email: [email protected]
Blood pressure
RUNNING HEAD RECTO PAGES
Chapter 30
Blood pressure
CHAPTER CONTENTS Introduction 305 Control of blood pressure 306 Hypertension 308 Hypotension 308 Osteopathic considerations 308 References 311
INTRODUCTION The term blood pressure means ‘the force exerted by the blood against any unit area of the vessel wall’.1 Conventionally it is measured in millimetres of mercury and expressed as two figures, the first representing the systolic reading and the second, the diastolic reading. If there is such a thing as a normal blood pressure, then the accepted value for a resting, healthy adult is 120/80 mmHg. However, there may be significant deviation and the values may increase or decrease with various circumstances, for example age, physical exertion, psychoemotional stress and certain pathological disease states. The above description of blood pressure and normal values are of the arterial blood pressure. Since the cardiovascular system is a closed system, theoretically it is possible to measure the pressure at any point throughout the whole system. Naturally enough, since the heart is the driving force and also since the aorta and its major branches are the first of the vessels in the system, it is here that we find the highest pressure. As the blood passes around the systemic circulatory system the blood pressure drops and the pulsatile effect diminishes. By the time the blood leaves the arterioles and enters the capillary beds, the pressure has dropped to about 30 mmHg and there is almost no perceivable pulsation. Throughout the capillary beds the pressure drops further and on reaching the venules it has reduced to about 10 mmHg; by the time it reaches the vena cavae and returns to the heart again it is at about 0 mmHg.1 Another consideration to be made is that of the hydrostatic pressure placed upon the blood in
305
306
CLINICAL CONDITIONS
the venous system. In the normal adult, the blood pressure of the veins varies from about 10 mmHg to zero. In the normal adult standing absolutely still, the pressure varies from the head to the feet as a result of the hydrostatic effect. Pressure in the venous sinuses of the head will be about –10 mmHg and in the feet about 90 mmHg, an appreciable variation due simply to the weight of the fluid in the system.1 This would tend to create a pooling of the blood in the lower extremities and so to minimize this effect the veins are equipped with a one-way valve system, directing the blood back to the heart. Muscular contraction, on walking or moving, puts pressure on the veins and literally squeezes the blood back to the heart. Failure of this system for too long a period of time may result in varicose veins. Furthermore, in the case of standing still, fluid leaks from the circulatory system into the surrounding tissues and creates oedema and thus swollen ankles or legs. It is the relative immobility leading to a reduction of the muscular pumping action that is the culprit, and so the same phenomenon may occur during long periods of sitting, as is commonly seen in travelling. Air travel makes the problem even worse due to reduced cabin air pressure. The pulmonary system is a law unto itself; it requires a certain amount of blood pressure to drive the blood through the lungs for gaseous exchange to take place but not too great a pressure to create leakage or extravasation of the fluids into the interstitial spaces or the alveoli resulting in pulmonary oedema. Normal resting pulmonary blood pressure varies from about 22 mmHg at systole to about 8 mmHg at diastole.1 Once again in the standing adult at rest there is a variation due to the hydrostatic pressure of about 3 mmHg in the apex of the lungs and 21 mmHg at the bases, indicating a variation in the blood flow throughout different regions of the lungs.1
CONTROL OF BLOOD PRESSURE The term ‘mean arterial pressure’ refers to the average pressure throughout each cycle of the heart and is ‘approximately’ equal to the average of the systolic and diastolic blood pressures. In fact, it is usually a little below this average due to the longer phase of diastole. Mean arterial pressure is dependent on the product of the cardiac output and the peripheral resistance.
Arterial pressure = cardiac output × total peripheral resistance The regulation of the mean arterial blood pressure is carried out by two different but related mechanisms, one for short-term regulation and the other for long-term regulation. It should also be remembered that there is a system of local blood flow regulation carried out at a tissue level by merely dilating or constricting the arterioles as required by the organ concerned. Short-term regulation is controlled by the nervous and hormonal systems whilst longer term regulation is by regulating the blood volume and involves the kidney. The fast acting mechanisms for control of blood pressure are mediated by the baroreceptor reflex (Fig. 30.1). Baroreceptors are stretch receptors located in the walls of major arteries but notably in the carotid sinus at the bifurcation of the common carotid arteries and in the arch of the aorta. Increased pressure creates increased stretch which is then transmitted as nervous impulses via Hering’s nerve to the glossopharyngeal nerve (from the carotid sinus) and vagus nerve (from the aortic arch) and thence to the nucleus of the tractus solitarius. From there, fibres pass to the reticular formation of the brain stem in a region known as the cardiovascular centre. The efferents from this centre then pass to the nucleus ambiguus and then by the vagus nerve to reduce the chronotropic and inotropic function of the heart, i.e. to reduce the rate and strength of contraction and thus cardiac output. Other fibres pass to the vasoconstrictor centre in order to inhibit the action of the sympathetics via the intermediolateral cell column of the spinal cord. The net effect is a reduction of mean arterial pressure. Naturally enough, should there be a drop in the blood pressure being monitored in this way, the opposite sequence of events will occur. These mechanisms are sufficient for the rapidly adapting needs of the body in response to short-term changes in pressure such as that seen in going from lying to standing, onset of exercise and loss of blood. The higher centres can have an influence on this system, for example, the response of increased blood pressure during the fight/flight response. However, this mechanism is not only rapidly acting but also fairly rapidly adapting, and so the baroreceptors become less sensitive and adapt to a sustained higher or lower blood pressure within a few days. Aside from the above described neural mechanism for rapid control of blood pressure is the
Blood pressure
Figure 30.1 The baroreceptor reflex nervous pathways. (Reproduced from Wilson-Pauwels L, Stewart PA, Akesson EJ. Autonomic nerves. Hamilton: BC Decker; 1997:205.)
relatively slower acting hormonal mechanism, principally the adrenaline-noradrenaline system and the renin-angiotensin system. Though the hormones take a little longer to effect a change they back up the neural mechanism.
Adrenaline and noradrenaline are two of the neurotransmitters utilized by the sympathetic nervous system which quite simply when activated stimulate a rise in blood pressure due to their vasoconstrictive action. Regulation of these hormones in
307
308
CLINICAL CONDITIONS
the blood gives a certain amount of control over blood pressure. However, the renin-angiotensin system utilizes angiotensin II which until fairly recently was considered the most powerful vasoconstrictor known in the body. Nowadays it is considered ‘one’ of the most powerful vasoconstrictors. Nevertheless its mechanism is a very potent one involving (as is the case in most hormonal mechanisms) a cascade reaction. In a very simplified version of the whole response, a reduction of blood pressure results in the release of renin from the kidney; this then activates the release of angiotensin I which is converted in the lungs to angiotensin II. Angiotensin has a short half-life but a rapid effect, notably causing a vasoconstriction of the arterioles, which increases peripheral resistance and thus raises the blood pressure. Furthermore, it effects a response in the kidneys; firstly it causes a reduction in the excretion of salt and water, thus increasing blood volume, and secondly it promotes the release of aldosterone that further reinforces this same effect. These latter effects are important in the shortto mid-term regulation of blood pressure but, more importantly, it is this system that controls the blood pressure in the longer term.
HYPERTENSION Butterworths Medical Dictionary2 describes hypertension as ‘high arterial blood pressure’: it then goes on to describe sixteen different types of hypertension! Aetiologically, hypertension can be divided into two major groups: primary and secondary. Primary hypertension is sometimes known as essential hypertension and is defined as that which arises from no known cause. Secondary hypertension may be due to numerous causes ranging from kidney disorders to tumours to iatrogenic causes. Hypertension is also classified according to the pathological changes it creates in the body. Benign hypertension, which usually includes essential hypertension, may create little or no demonstrable system or organ damage. On the other hand, malignant hypertension results in serious damage and an increased risk of death from numerous causes.
HYPOTENSION Butterworths Medical Dictionary2 describes hypotension as ‘a fall in blood pressure below the normal
range’; it then goes on to describe four different types of hypotension. It is evident that the greater risks to health come from hypertension but nevertheless, hypotension is potentially deleterious to the health and as such deserves a mention. By far the most commonly seen form of hypotension is postural or orthostatic. This is due to an inefficient response to blood pressure changes on going from sitting or lying to the standing position. It manifests as dizziness, blurred vision or even syncope. It is due to a lack of the normal autonomic responses required in the short-term changes as mentioned earlier. It may be transient or persistent and is named ‘acute’ or ‘chronic’ accordingly. Its causes vary from starvation and physical exhaustion, through immobility, to specific diseases such as diabetes mellitus, adrenal insufficiency and intracranial tumours.
OSTEOPATHIC CONSIDERATIONS As may be seen from the above discussion, there are two major systems of importance in the control of blood pressure, the nervous control and that of the endocrine effect on the kidneys. Thus any osteopath attempting to treat a patient with hypertension will need to check for any dysfunctions related to these two systems. Firstly, the kidneys are to be found in a ‘nest’ of perirenal adipose tissue on the internal aspect of the posterior abdominal wall. Their anatomical relations are numerous and varied3 (Fig. 30.2). The right kidney is related anteriorly to the suprarenal gland, the liver, the second part of the duodenum and the right colic flexure. Posteriorly it is related to the diaphragm, the costodiaphragmatic recess of the pleura and the twelfth rib, the psoas, quadratus lumborum and transversus abdominis muscles and the subcostal, iliohypogastric and ilioinguinal nerves. The left kidney is related anteriorly to the suprarenal gland, spleen, stomach, pancreas, left colic flexure and jejunum. Posteriorly its relations are to the same but contralateral structures as the right kidney with the addition of the eleventh rib – this is due to the left kidney lying slightly higher in position. Evidently, with all these anatomical relations, there is always the possibility of dysfunction that may compromise normal function of the kidneys. The anatomical arrangement is that of visceral structures anterior to the kidneys and with that goes all the ‘sliding surfaces’ necessary for normal
Blood pressure
Figure 30.2 (A) Anterior and (B) posterior relations of the kidneys.
mobility. However with all the musculoskeletal elements posteriorly, and the effect of the diaphragm, there are many non-visceral aspects to be considered. So no matter which ‘direction’ the osteopath is coming from, there is the possibility to treat dysfunction. It should also not be forgotten that the kidneys receive their sympathetic supply from the T10–L2 spinal cord levels thus making the dorsolumbar junction a very important area in the consideration of these types of problems. Barral4 writes that kidney mobility and motility are important considerations in hypertensive patients and thus should be checked for any dysfunction and
treated accordingly. Kidney ‘ptosis’ may occur, in which the kidney descends or slips down within its fascial sheath that is lying on the psoas major muscle. Athletes and serious runners are especially susceptible to this type of problem due to the repetitive jarring from training coupled with the fact that a serious runner probably has a minimal amount of fat acting as a support for the kidneys. Barral4 cites the case of an extremely hypertensive young lady who was diagnosed as having idiopathic hypertension. She was treated osteopathically for a left renal ptosis and her blood pressure reduced quite rapidly. It is his thought that osteopathic treatment does not restore the ptosed
309
310
CLINICAL CONDITIONS
kidney to its correct position, rather the treatment is successful due to ‘stimulation, dynamization and revitalization of the organism’. In other words, the kidney is given the space in which to restore its normal homeostatic functions. William Baldwin Jnr5 writes in the classic text Osteopathic Medicine edited by Hoag, Cole and Bradford, that ‘renal function must be involved in the hypertensive process, sooner or later’ and that ‘the longer optimum renal function can be maintained, the better the patient’s chances for avoiding the extreme complications’. He goes on to say that ‘one of the best hypotensive agents is sedation’ and that ‘generalised manipulative therapy has just such an effect’. This underlines the oft-neglected principle that there should be a treatment of the person and not merely the pathological condition. Since stress is often implicated in hypertension, a general treatment that may result in the reduction of circulating stress hormones to normal levels may be considered as a means of approaching hypertension either directly or indirectly. Pain is associated with higher levels of catecholamines and thus higher blood pressure. The osteopathic means of pain reduction is likely to result in a reduction of blood pressure. The relationship between pain, range of joint motion and stress is quite significantly correlated and it is the osteopathic approach which may have the beneficial effect.6 The baroreceptor reflex has been the subject for some osteopathic studies with respect to blood pressure but as mentioned, this reflex is more important in the short term and although important will be less so in the longer term control. However, this reflex is coordinated via the circulatory centres of the brain stem which are lying just deep to the floor of the fourth ventricle. It is with this in mind that many osteopaths direct part of their treatment to this region. Magoun7 states that ‘persistent use of compression of the fourth ventricle to influence the centers for blood pressure in its floor, as well as vault lift for better venous drainage, is often of help in altering tissue chemistry and stagnation sufficiently to maintain the pressure at a safe level’. Unfortunately, as is often the case in osteopathy, there are numerous anecdotal accounts of a reduction in blood pressure in patients treated osteopathically but few controlled trials. However, a recent study8 concluded that long-term manipulation to the T2–3 and T11–12 may provide decreases in both systolic and diastolic blood pressures in hyperten-
sive patients. Unfortunately the subject population was very small and, as is often stated, further investigations with larger populations are required and in the case of this particular research, a longer-term study and follow-up. In the 1955 Yearbook of the Applied Academy of Osteopathy, Northup9 describes his method for management of hypertension and although he recognizes the necessity to work on any vertebral restrictions, notably those related to kidney or liver, he also describes ‘cranial technique’. It involves releasing all the tissues around the suboccipital region and the cervical fascia, followed by easing restrictions of the temporal bones and especially the occipitomastoid sutures. He states the importance of the meninges and their attachments within the cranial vault. A major part of his treatment approach is aimed at relaxation of the tissues and of the person as a whole, two important factors known to aid in the reduction of mean arterial pressure. Northup cites a modification of his technique used by Dr Paul C Snyder that ‘has had outstanding results’ and which involves a type of mild but sustained traction to the cervical fascia (Northup used a rocking motion in this region). Snyder felt that the success of the technique was due to a stretching of the carotid sheath and inhibitory influence on the carotid sinus, a claim that is quite feasible when considering short-term changes. Earlier still, McCole10 wrote in the 1951 Yearbook of the Applied Academy of Osteopathy that the suboccipital triangle is important, as are the first, second and fifth thoracic segments, in order to maintain normal autonomic balance. He also makes mention of the importance of the kidney and of psychosocial aspects of the patient’s lifestyle including: alcohol, tobacco and coffee consumption. It would seem that osteopathy does have something to offer towards the treatment and management of hypertensive patients. The anatomical regions highlighted earlier are undoubtedly of importance and the osteopathic holistic approach will further reinforce this effect. The management of a person with hypertension will necessitate examination of diet and lifestyle in addition to the physical side of treatment. Osteopathic treatment and management of the hypertensive patient should not be considered as an alternative to medication but as an adjunct to it which may result in shorter-term medication or possibly a reduced dosage.
Blood pressure
References 1. Guyton AC, Hall JE. Textbook of medical physiology, 10th edn. Philadelphia: WB Saunders; 2000. 2. Butterworths Medical Dictionary, 2nd edn. London: Butterworths; 1989. 3. Williams PL, Warwick R. Gray’s anatomy, 36th edn. Edinburgh: Churchill Livingstone; 1980. 4. Barral JP. Visceral manipulation II. Seattle: Eastland Press; 1989. 5. Baldwin W. Hypertension. In: Hoag JM, Cole WV, Bradford SG, eds. Osteopathic medicine. New York: McGraw-Hill; 1969:519–528. 6. Marcer N. Osteopathy in the treatment of stress. Abstract. J Ost Med 2003; 6(1):34–42.
7. Magoun HI. Osteopathy in the cranial field. Boise: Northwest Printing; 1976. 8. Morden J, Gosling CM, Cameron M. The effect of thoracic manipulation on blood pressure in pharmacologically stable patients with hypertension: a pilot investigation. Abstract. J Ost Med 2003; 6(1). 9. Northup TL. Manipulative therapy in the osteopathic management of hypertension. Applied Academy of Osteopathy Yearbook; 1957. 10. McCole G. Clinical aspects of blood pressure determination. Applied Academy of Osteopathy Yearbook; 1951.
311
Chapter 30
Blood pressure
CHAPTER CONTENTS Introduction 305 Control of blood pressure 306 Hypertension 308 Hypotension 308 Osteopathic considerations 308 References 311
INTRODUCTION The term blood pressure means ‘the force exerted by the blood against any unit area of the vessel wall’.1 Conventionally it is measured in millimetres of mercury and expressed as two figures, the first representing the systolic reading and the second, the diastolic reading. If there is such a thing as a normal blood pressure, then the accepted value for a resting, healthy adult is 120/80 mmHg. However, there may be significant deviation and the values may increase or decrease with various circumstances, for example age, physical exertion, psychoemotional stress and certain pathological disease states. The above description of blood pressure and normal values are of the arterial blood pressure. Since the cardiovascular system is a closed system, theoretically it is possible to measure the pressure at any point throughout the whole system. Naturally enough, since the heart is the driving force and also since the aorta and its major branches are the first of the vessels in the system, it is here that we find the highest pressure. As the blood passes around the systemic circulatory system the blood pressure drops and the pulsatile effect diminishes. By the time the blood leaves the arterioles and enters the capillary beds, the pressure has dropped to about 30 mmHg and there is almost no perceivable pulsation. Throughout the capillary beds the pressure drops further and on reaching the venules it has reduced to about 10 mmHg; by the time it reaches the vena cavae and returns to the heart again it is at about 0 mmHg.1 Another consideration to be made is that of the hydrostatic pressure placed upon the blood in
305
306
CLINICAL CONDITIONS
the venous system. In the normal adult, the blood pressure of the veins varies from about 10 mmHg to zero. In the normal adult standing absolutely still, the pressure varies from the head to the feet as a result of the hydrostatic effect. Pressure in the venous sinuses of the head will be about –10 mmHg and in the feet about 90 mmHg, an appreciable variation due simply to the weight of the fluid in the system.1 This would tend to create a pooling of the blood in the lower extremities and so to minimize this effect the veins are equipped with a one-way valve system, directing the blood back to the heart. Muscular contraction, on walking or moving, puts pressure on the veins and literally squeezes the blood back to the heart. Failure of this system for too long a period of time may result in varicose veins. Furthermore, in the case of standing still, fluid leaks from the circulatory system into the surrounding tissues and creates oedema and thus swollen ankles or legs. It is the relative immobility leading to a reduction of the muscular pumping action that is the culprit, and so the same phenomenon may occur during long periods of sitting, as is commonly seen in travelling. Air travel makes the problem even worse due to reduced cabin air pressure. The pulmonary system is a law unto itself; it requires a certain amount of blood pressure to drive the blood through the lungs for gaseous exchange to take place but not too great a pressure to create leakage or extravasation of the fluids into the interstitial spaces or the alveoli resulting in pulmonary oedema. Normal resting pulmonary blood pressure varies from about 22 mmHg at systole to about 8 mmHg at diastole.1 Once again in the standing adult at rest there is a variation due to the hydrostatic pressure of about 3 mmHg in the apex of the lungs and 21 mmHg at the bases, indicating a variation in the blood flow throughout different regions of the lungs.1
CONTROL OF BLOOD PRESSURE The term ‘mean arterial pressure’ refers to the average pressure throughout each cycle of the heart and is ‘approximately’ equal to the average of the systolic and diastolic blood pressures. In fact, it is usually a little below this average due to the longer phase of diastole. Mean arterial pressure is dependent on the product of the cardiac output and the peripheral resistance.
Arterial pressure = cardiac output × total peripheral resistance The regulation of the mean arterial blood pressure is carried out by two different but related mechanisms, one for short-term regulation and the other for long-term regulation. It should also be remembered that there is a system of local blood flow regulation carried out at a tissue level by merely dilating or constricting the arterioles as required by the organ concerned. Short-term regulation is controlled by the nervous and hormonal systems whilst longer term regulation is by regulating the blood volume and involves the kidney. The fast acting mechanisms for control of blood pressure are mediated by the baroreceptor reflex (Fig. 30.1). Baroreceptors are stretch receptors located in the walls of major arteries but notably in the carotid sinus at the bifurcation of the common carotid arteries and in the arch of the aorta. Increased pressure creates increased stretch which is then transmitted as nervous impulses via Hering’s nerve to the glossopharyngeal nerve (from the carotid sinus) and vagus nerve (from the aortic arch) and thence to the nucleus of the tractus solitarius. From there, fibres pass to the reticular formation of the brain stem in a region known as the cardiovascular centre. The efferents from this centre then pass to the nucleus ambiguus and then by the vagus nerve to reduce the chronotropic and inotropic function of the heart, i.e. to reduce the rate and strength of contraction and thus cardiac output. Other fibres pass to the vasoconstrictor centre in order to inhibit the action of the sympathetics via the intermediolateral cell column of the spinal cord. The net effect is a reduction of mean arterial pressure. Naturally enough, should there be a drop in the blood pressure being monitored in this way, the opposite sequence of events will occur. These mechanisms are sufficient for the rapidly adapting needs of the body in response to short-term changes in pressure such as that seen in going from lying to standing, onset of exercise and loss of blood. The higher centres can have an influence on this system, for example, the response of increased blood pressure during the fight/flight response. However, this mechanism is not only rapidly acting but also fairly rapidly adapting, and so the baroreceptors become less sensitive and adapt to a sustained higher or lower blood pressure within a few days. Aside from the above described neural mechanism for rapid control of blood pressure is the
Blood pressure
Figure 30.1 The baroreceptor reflex nervous pathways. (Reproduced from Wilson-Pauwels L, Stewart PA, Akesson EJ. Autonomic nerves. Hamilton: BC Decker; 1997:205.)
relatively slower acting hormonal mechanism, principally the adrenaline-noradrenaline system and the renin-angiotensin system. Though the hormones take a little longer to effect a change they back up the neural mechanism.
Adrenaline and noradrenaline are two of the neurotransmitters utilized by the sympathetic nervous system which quite simply when activated stimulate a rise in blood pressure due to their vasoconstrictive action. Regulation of these hormones in
307
308
CLINICAL CONDITIONS
the blood gives a certain amount of control over blood pressure. However, the renin-angiotensin system utilizes angiotensin II which until fairly recently was considered the most powerful vasoconstrictor known in the body. Nowadays it is considered ‘one’ of the most powerful vasoconstrictors. Nevertheless its mechanism is a very potent one involving (as is the case in most hormonal mechanisms) a cascade reaction. In a very simplified version of the whole response, a reduction of blood pressure results in the release of renin from the kidney; this then activates the release of angiotensin I which is converted in the lungs to angiotensin II. Angiotensin has a short half-life but a rapid effect, notably causing a vasoconstriction of the arterioles, which increases peripheral resistance and thus raises the blood pressure. Furthermore, it effects a response in the kidneys; firstly it causes a reduction in the excretion of salt and water, thus increasing blood volume, and secondly it promotes the release of aldosterone that further reinforces this same effect. These latter effects are important in the shortto mid-term regulation of blood pressure but, more importantly, it is this system that controls the blood pressure in the longer term.
HYPERTENSION Butterworths Medical Dictionary2 describes hypertension as ‘high arterial blood pressure’: it then goes on to describe sixteen different types of hypertension! Aetiologically, hypertension can be divided into two major groups: primary and secondary. Primary hypertension is sometimes known as essential hypertension and is defined as that which arises from no known cause. Secondary hypertension may be due to numerous causes ranging from kidney disorders to tumours to iatrogenic causes. Hypertension is also classified according to the pathological changes it creates in the body. Benign hypertension, which usually includes essential hypertension, may create little or no demonstrable system or organ damage. On the other hand, malignant hypertension results in serious damage and an increased risk of death from numerous causes.
HYPOTENSION Butterworths Medical Dictionary2 describes hypotension as ‘a fall in blood pressure below the normal
range’; it then goes on to describe four different types of hypotension. It is evident that the greater risks to health come from hypertension but nevertheless, hypotension is potentially deleterious to the health and as such deserves a mention. By far the most commonly seen form of hypotension is postural or orthostatic. This is due to an inefficient response to blood pressure changes on going from sitting or lying to the standing position. It manifests as dizziness, blurred vision or even syncope. It is due to a lack of the normal autonomic responses required in the short-term changes as mentioned earlier. It may be transient or persistent and is named ‘acute’ or ‘chronic’ accordingly. Its causes vary from starvation and physical exhaustion, through immobility, to specific diseases such as diabetes mellitus, adrenal insufficiency and intracranial tumours.
OSTEOPATHIC CONSIDERATIONS As may be seen from the above discussion, there are two major systems of importance in the control of blood pressure, the nervous control and that of the endocrine effect on the kidneys. Thus any osteopath attempting to treat a patient with hypertension will need to check for any dysfunctions related to these two systems. Firstly, the kidneys are to be found in a ‘nest’ of perirenal adipose tissue on the internal aspect of the posterior abdominal wall. Their anatomical relations are numerous and varied3 (Fig. 30.2). The right kidney is related anteriorly to the suprarenal gland, the liver, the second part of the duodenum and the right colic flexure. Posteriorly it is related to the diaphragm, the costodiaphragmatic recess of the pleura and the twelfth rib, the psoas, quadratus lumborum and transversus abdominis muscles and the subcostal, iliohypogastric and ilioinguinal nerves. The left kidney is related anteriorly to the suprarenal gland, spleen, stomach, pancreas, left colic flexure and jejunum. Posteriorly its relations are to the same but contralateral structures as the right kidney with the addition of the eleventh rib – this is due to the left kidney lying slightly higher in position. Evidently, with all these anatomical relations, there is always the possibility of dysfunction that may compromise normal function of the kidneys. The anatomical arrangement is that of visceral structures anterior to the kidneys and with that goes all the ‘sliding surfaces’ necessary for normal
Blood pressure
Figure 30.2 (A) Anterior and (B) posterior relations of the kidneys.
mobility. However with all the musculoskeletal elements posteriorly, and the effect of the diaphragm, there are many non-visceral aspects to be considered. So no matter which ‘direction’ the osteopath is coming from, there is the possibility to treat dysfunction. It should also not be forgotten that the kidneys receive their sympathetic supply from the T10–L2 spinal cord levels thus making the dorsolumbar junction a very important area in the consideration of these types of problems. Barral4 writes that kidney mobility and motility are important considerations in hypertensive patients and thus should be checked for any dysfunction and
treated accordingly. Kidney ‘ptosis’ may occur, in which the kidney descends or slips down within its fascial sheath that is lying on the psoas major muscle. Athletes and serious runners are especially susceptible to this type of problem due to the repetitive jarring from training coupled with the fact that a serious runner probably has a minimal amount of fat acting as a support for the kidneys. Barral4 cites the case of an extremely hypertensive young lady who was diagnosed as having idiopathic hypertension. She was treated osteopathically for a left renal ptosis and her blood pressure reduced quite rapidly. It is his thought that osteopathic treatment does not restore the ptosed
309
310
CLINICAL CONDITIONS
kidney to its correct position, rather the treatment is successful due to ‘stimulation, dynamization and revitalization of the organism’. In other words, the kidney is given the space in which to restore its normal homeostatic functions. William Baldwin Jnr5 writes in the classic text Osteopathic Medicine edited by Hoag, Cole and Bradford, that ‘renal function must be involved in the hypertensive process, sooner or later’ and that ‘the longer optimum renal function can be maintained, the better the patient’s chances for avoiding the extreme complications’. He goes on to say that ‘one of the best hypotensive agents is sedation’ and that ‘generalised manipulative therapy has just such an effect’. This underlines the oft-neglected principle that there should be a treatment of the person and not merely the pathological condition. Since stress is often implicated in hypertension, a general treatment that may result in the reduction of circulating stress hormones to normal levels may be considered as a means of approaching hypertension either directly or indirectly. Pain is associated with higher levels of catecholamines and thus higher blood pressure. The osteopathic means of pain reduction is likely to result in a reduction of blood pressure. The relationship between pain, range of joint motion and stress is quite significantly correlated and it is the osteopathic approach which may have the beneficial effect.6 The baroreceptor reflex has been the subject for some osteopathic studies with respect to blood pressure but as mentioned, this reflex is more important in the short term and although important will be less so in the longer term control. However, this reflex is coordinated via the circulatory centres of the brain stem which are lying just deep to the floor of the fourth ventricle. It is with this in mind that many osteopaths direct part of their treatment to this region. Magoun7 states that ‘persistent use of compression of the fourth ventricle to influence the centers for blood pressure in its floor, as well as vault lift for better venous drainage, is often of help in altering tissue chemistry and stagnation sufficiently to maintain the pressure at a safe level’. Unfortunately, as is often the case in osteopathy, there are numerous anecdotal accounts of a reduction in blood pressure in patients treated osteopathically but few controlled trials. However, a recent study8 concluded that long-term manipulation to the T2–3 and T11–12 may provide decreases in both systolic and diastolic blood pressures in hyperten-
sive patients. Unfortunately the subject population was very small and, as is often stated, further investigations with larger populations are required and in the case of this particular research, a longer-term study and follow-up. In the 1955 Yearbook of the Applied Academy of Osteopathy, Northup9 describes his method for management of hypertension and although he recognizes the necessity to work on any vertebral restrictions, notably those related to kidney or liver, he also describes ‘cranial technique’. It involves releasing all the tissues around the suboccipital region and the cervical fascia, followed by easing restrictions of the temporal bones and especially the occipitomastoid sutures. He states the importance of the meninges and their attachments within the cranial vault. A major part of his treatment approach is aimed at relaxation of the tissues and of the person as a whole, two important factors known to aid in the reduction of mean arterial pressure. Northup cites a modification of his technique used by Dr Paul C Snyder that ‘has had outstanding results’ and which involves a type of mild but sustained traction to the cervical fascia (Northup used a rocking motion in this region). Snyder felt that the success of the technique was due to a stretching of the carotid sheath and inhibitory influence on the carotid sinus, a claim that is quite feasible when considering short-term changes. Earlier still, McCole10 wrote in the 1951 Yearbook of the Applied Academy of Osteopathy that the suboccipital triangle is important, as are the first, second and fifth thoracic segments, in order to maintain normal autonomic balance. He also makes mention of the importance of the kidney and of psychosocial aspects of the patient’s lifestyle including: alcohol, tobacco and coffee consumption. It would seem that osteopathy does have something to offer towards the treatment and management of hypertensive patients. The anatomical regions highlighted earlier are undoubtedly of importance and the osteopathic holistic approach will further reinforce this effect. The management of a person with hypertension will necessitate examination of diet and lifestyle in addition to the physical side of treatment. Osteopathic treatment and management of the hypertensive patient should not be considered as an alternative to medication but as an adjunct to it which may result in shorter-term medication or possibly a reduced dosage.
Blood pressure
References 1. Guyton AC, Hall JE. Textbook of medical physiology, 10th edn. Philadelphia: WB Saunders; 2000. 2. Butterworths Medical Dictionary, 2nd edn. London: Butterworths; 1989. 3. Williams PL, Warwick R. Gray’s anatomy, 36th edn. Edinburgh: Churchill Livingstone; 1980. 4. Barral JP. Visceral manipulation II. Seattle: Eastland Press; 1989. 5. Baldwin W. Hypertension. In: Hoag JM, Cole WV, Bradford SG, eds. Osteopathic medicine. New York: McGraw-Hill; 1969:519–528. 6. Marcer N. Osteopathy in the treatment of stress. Abstract. J Ost Med 2003; 6(1):34–42.
7. Magoun HI. Osteopathy in the cranial field. Boise: Northwest Printing; 1976. 8. Morden J, Gosling CM, Cameron M. The effect of thoracic manipulation on blood pressure in pharmacologically stable patients with hypertension: a pilot investigation. Abstract. J Ost Med 2003; 6(1). 9. Northup TL. Manipulative therapy in the osteopathic management of hypertension. Applied Academy of Osteopathy Yearbook; 1957. 10. McCole G. Clinical aspects of blood pressure determination. Applied Academy of Osteopathy Yearbook; 1951.
311