Blood Pressure – Role of pharmacists in hypertension

Blood pressure
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Blood pressure (BP) is the pressure of circulating blood on the walls of blood vessels. Used without further specification, “blood pressure” usually refers to the pressure in large arteries of the systemic circulation. Blood pressure is usually expressed in terms of the systolic pressure (maximum during one heartbeat) over diastolic pressure (minimum in between two heartbeats) and is measured in millimeters of mercury (mmHg), above the surrounding atmospheric pressure (considered to be zero for convenience).

Considering the increasingly clinical roles pharmacists are taking on, the ability to accurately take and interpret blood pressure has never been more important. A study in the Journal of Hypertension compared community pharmacy blood pressure measurements with measurements taken in GP clinics and other settings in the same patients, to establish a clearer picture of how they might differ.

Hypertension is the most common, preventable risk factor for cardiovascular events worldwide, and affects almost a third of all adults in England. Epidemiological data suggest that a 10mmHg reduction in systolic blood pressure (BP) across the population, regardless of baseline cardiovascular risk, could result in a 41% reduction in risk of stroke and 22% reduction in coronary heart disease. Despite this, only half of the diagnosed hypertensive patients on treatment are deemed to have adequately controlled BP. Largely because of its asymptomatic nature, Public Health England (PHE) estimates that around 5.6 million adults in England are unaware of having elevated BP — these individuals are known as ‘undiagnosed hypertensives’.

In September 2017, community pharmacies up and down the country offered free BP checks to thousands of members of the public as part of ‘know your numbers’ week. In preparation, the staff at the Oxfordshire pharmacy where I practice, were keen to know more about BP measurement protocols; how to interpret the readings they were about to obtain; and what advice to give patients.

In the October 2017 issue of the Journal of Hypertension, we presented a systematic review and meta-analysis of published evidence that aimed to answer some of these questions. The study compared community pharmacy blood pressure (CPBP) measurements with general practitioner (GP) clinic, home blood pressure monitoring (HBPM) and ambulatory blood pressure monitoring (ABPM) readings in the same patients.

Evidence for the role of pharmacists in hypertension care

There is sufficient evidence to suggest that pharmacist management, or pharmacist and GP co-management, of hypertension, can reduce BP compared with usual care alone. For instance, a systematic review of randomized controlled trials identified 16 studies of ‘community pharmacist interventions on control of BP in hypertensive patients’. The nature of the interventions across the studies included: establishing and improving adherence to BP medications; early identification of drug-related problems and side effects; optimal drug selection for individual patients; and practical diet and lifestyle advice, including stop-smoking schemes.

Across the studies, systolic BP reduction in the pharmacy intervention arms were clinically significant, showing a -6.1mmHg (95% confidence interval (CI): -8.4 to -3.8) difference compared with usual GP care. To provide some context, an antihypertensive drug such as a thiazide diuretic, prescribed at a normal maintenance dose, is expected to decrease systolic BP by 8mmHg on average.

Furthermore, targeted cardiovascular risk assessments in pharmacies have shown potential in screening and referring high-risk patients to general practice.

Considering this information, and the increasingly clinical roles pharmacists are taking on, the ability to accurately take and interpret BP has never been more important.

Standardizing blood pressure measurements in pharmacies

Variations in BP measurement techniques can have a substantial effect on blood pressure readings and, consequently, clinical decisions. Table 1 shows some of the common factors that can influence BP readings and their estimated effect on the results.

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In our review, mean CPBP was calculated from a wide range of visits to the pharmacy (one to five visits) as well as from a range of repeat readings taken per visit (two to six readings) within each study. Furthermore, the protocol for calculating the mean (whether the first reading is discarded) and the member of the pharmacy team taking the readings varied.

The effects of these differences were partially reflected in the systolic BP comparisons, which suggested that the more readings and repeat visits, the closer the correlation between pharmacy and out-of-office measurements. Higher numbers of repeat readings have been shown to lead to a ‘regression to the mean’ effect and hence a closer relationship to the multiple readings taken via HBPM and ABPM.

Table 1: Common factors that can affect blood pressure during consultations
FactorsEstimated average effect on systolic blood pressure (mmHg)
Patient talking during the measurement+17
Full bladder/urge to urinate during the measurement+15
Consumption of alcohol in the three hours prior to reading+8
Legs crossed during readings+7
Observed reading vs unattended reading (patient alone in the consultation room)+5 to +16
Consumption of caffeinated drink one hour prior to reading+3 to +15
Cuff one size too small+2 to +6
No arm support during reading.+2

The differences in the way BP was measured across the studies highlighted the fact that, currently, neither the Royal Pharmaceutical Society (RPS) nor the World Health Organization (WHO) recommends a standardized protocol for the measurement of blood pressure in pharmacies,

With workloads in pharmacies increasing, requesting that patients return to the pharmacy on several occasions within a short period of time may not be convenient for either party. Equally, taking up to six repeated BP measurements (with a one-minute break between each) may be time-consuming and not conducive to effective overall consultation. Therefore our study recommends a pragmatic approach to measurements, involving triplicate readings, discarding the first reading and taking an average of measurements two and three when the initial reading is deemed high.

Some studies used non-validated monitors to estimate CPBP, such as wrist devices We encourage pharmacy teams and patients to ensure that their BP monitors are validated by verifying on the British and Irish Hypertension Society website, and ensuring manual devices are used for patients with atrial fibrillation.

Interpreting readings were taken in pharmacies

How should we interpret BP readings taken in pharmacies? Thresholds of 140/90mmHg (GP clinic) and 135/85mmHg (daytime ABPM/HBPM) are currently adopted for hypertension diagnosis and management among non-diabetic adults under the age of 80 years. The RPS and the WHO have previously recommended the 140/90mmHg threshold for the diagnosis of elevated blood pressure in pharmacies. This threshold, however, is based on the assumption that pharmacies, as clinically related settings, are associated with the same ‘white coat effect’ as GP clinics, rather than on diagnostic accuracy or comparison studies.

(Pooled analysis in our systematic review showed no significant difference between CPBP and daytime ABPM readings (mean difference 1.6mmHg (95% CI: -1.2 to 4.3)), and that mean BPs recorded in pharmacies were significantly higher than 24-hour ABPM readings (mean difference 7.8mmHg (95% CI: 1.5 to 14.1)). In other words, pharmacy readings were shown to be no different to daytime ABPM readings, and higher than 24-hour ABPM readings. This pattern was further confirmed with the CPBP/HBPM comparison (mean difference 2.4mmHg (95% CI: 0.0 to 4.8)) where no clinically significant difference (±5mmHg) was observed.

The three comparisons above indicate that CPBP may be best interpreted using out-of-office BP thresholds (i.e. 135/85mmHg) rather than the commonly adopted 140/90mmHg clinic threshold. In keeping with this interpretation, we would expect CPBP readings to be significantly lower than GP clinic measurements; however, this was not observed and no significant difference was found (mean difference -0.9mmHg (95% CI: -3.5 to +1.7)).

The reasons for this inconsistency lie partly in the variety of BP measurements used in the studies. For example, only two of the six studies comparing GP clinic with pharmacy readings were taken by GPs themselves. The rest involved either nurses, research assistants or automated unattended measurements. To exemplify the potential impact of these differences, a systematic review demonstrated that clinic readings taken by nurses can be up to 7.0mmHg lower than GP-measured readings (95% CI: -4.7 to -9.2).

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Conclusion

Currently, elevated BP readings taken in community pharmacies result in either referral to a GP or advice to the patient, rather than formal diagnosis or regular monitoring. Given this context and the data collected, CPBP readings may be best interpreted using the home/daytime ABPM threshold for the diagnosis and management of hypertension (135/85mmHg).

This approach would likely result in higher sensitivity (true positive rate) for detecting hypertension when referring patients to their GP with borderline elevated BP, albeit at the expense of specificity (false positive rate). To avoid an increase in GP workload through inappropriate referral, pharmacies could consider directing patients toward home or daytime ABPM to further refine referral criteria after elevated CPBP readings.

Staff at the pharmacy where I practice were able to successfully engage with the ‘know your numbers’ week, offering blood pressure measurements and advice to help patients reduce their BP, and have continued to do this beyond the promotional week. If pharmacies can continue to demonstrate their value in hypertension detection and management, we hope that future service development can be focused on setting up the necessary infrastructure to formally allow pharmacists to manage patients with hypertension from community settings.

Systole on the left and diastole on the right

During each heartbeat, blood pressure varies between a maximum (systolic) and a minimum (diastolic) pressure. The blood pressure in the circulation is principally due to the pumping action of the heart. Differences in mean blood pressure are responsible for blood flow from one location to another in the circulation. The rate of mean blood flow depends on both blood pressure and the resistance to flow presented by the blood vessels. Mean blood pressure decreases as the circulating blood moves away from the heart through arteries and capillaries due to viscous losses of energy. Mean blood pressure drops over the whole circulation, although most of the fall occurs along the small arteries and arterioles. Gravity affects blood pressure via hydrostatic forces (e.g., during standing), and valves in veins, breathing, and pumping from contraction of skeletal muscles also influence blood pressure in veins.

Hemodynamics

Most influences on blood pressure can be understood in terms of their effect on cardiac output and resistance (the determinants of mean arterial pressure).

Some factors are:

  • Blood volume – the greater the blood volume, the higher the cardiac output. There is some relationship between dietary salt intake and increased blood volume, potentially resulting in higher arterial pressure, though this varies with the individual and is highly dependent on autonomic nervous system response and the renin–angiotensin system.
  • Cardiac output – the pumping action of the heart is ultimately responsible for blood pressure. Increases or decreases in cardiac output can result in increases or decreases respectively in blood pressure.
  • Systemic vascular resistance – the higher the resistance to blood flow, the higher the arterial pressure upstream needs to be to maintain flow. In simple terms, resistance is related to vessel radius by the Hagen-Poiseuille’s equation (resistance∝1/radius4, so the smaller the radius, the very much higher the resistance). Other physical factors that affect resistance include vessel length (the longer the vessel, the higher the resistance), blood viscosity (the higher the viscosity, the higher the resistance) and the presence of arterial stenosis (narrow stenosis increases resistance to flow, however this increase in resistance rarely if ever increases systemic blood pressure, it decreases downstream flow). Substances called vasoconstrictors can reduce the caliber of blood vessels, thereby increasing blood pressure. Vasodilators (such as nitroglycerin) increase the caliber of blood vessels, thereby decreasing arterial pressure.

In practice, each individual’s autonomic nervous system and other systems regulating blood pressure respond to and regulate all these factors so that, although the above issues are important, they rarely act in isolation and the actual arterial pressure response of a given individual can vary widely in the short and long term.

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Regulation

The endogenous regulation of arterial pressure is not completely understood, but the following mechanisms of regulating arterial pressure have been well-characterized:

  • Baroreceptor reflex – Baroreceptors in the high-pressure receptor zones detect changes in arterial pressure. These baroreceptors send signals ultimately to the medulla of the brain stem, specifically to the rostral ventrolateral medulla (RVLM). The medulla, by way of the autonomic nervous system, adjusts the mean arterial pressure by altering both the force and speed of the heart’s contractions, as well as the systemic vascular resistance. The most important arterial baroreceptors are located in the left and right carotid sinuses and in the aortic arch.
  • Renin-angiotensin system (RAS) – This system is generally known for its long-term adjustment of arterial pressure. This system allows the kidney to compensate for the loss in blood volume or drops in arterial pressure by activating an endogenous vasoconstrictor known as angiotensin II.
  • Aldosterone release –This steroid hormone is released from the adrenal cortex in response to angiotensin II or high serum potassium levels. Aldosterone stimulates sodium retention and potassium excretion by the kidneys. Since sodium is the main ion that determines the amount of fluid in the blood vessels by osmosis, aldosterone will increase fluid retention, and indirectly, arterial pressure.
  • Baroreceptors – in low-pressure receptor zones (mainly in the venae cavae and the pulmonary veins, and in the atria) result in feedback by regulating the secretion of antidiuretic hormone(ADH/Vasopressin), renin and aldosterone. The resultant increase in blood volume results in an increased cardiac output by the Frank-Starling law of the heart, in turn increasing arterial blood pressure.

These different mechanisms are not necessarily independent of each other, as indicated by the link between the RAS and aldosterone release. When blood pressure falls many physiological cascades commence in order to return the blood pressure to a more appropriate level.

  • The blood pressure fall is detected by a decrease in blood flow and thus a decrease in Glomerular filtration rate (GFR).
  • A decrease in GFR is sensed as a decrease in Na+ levels by the macula densa.
  • The macula densa causes an increase in Na+ reabsorption, which causes water to follow in via osmosis and leads to an ultimate increase in plasma volume. Further, the macula densa releases adenosine which causes constriction of the afferent arterioles.
  • At the same time, the juxtaglomerular cells sense the decrease in blood pressure and release renin.
  • Renin converts angiotensinogen (inactive form) to angiotensin I (active form).
  • Angiotensin I flows in the bloodstream until it reaches the capillaries of the lungs where angiotensin-converting enzyme (ACE) acts on it to convert it into angiotensin II.
  • Angiotensin II is a vasoconstrictor that will increase blood flow to the heart and subsequently the preload, ultimately increasing the cardiac output.
  • Angiotensin II also causes an increase in the release of aldosterone from the adrenal glands.
  • Aldosterone further increases the Na+ and H2O reabsorption in the distal convoluted tubule of the nephron.

Currently, the RAS is targeted pharmacologically by ACE inhibitors and angiotensin II receptor antagonists. The aldosterone system is directly targeted by spironolactone, an aldosterone antagonist. The fluid retention may be targeted by diuretics; the antihypertensive effect of diuretics is due to its effect on blood volume. Generally, the baroreceptor reflex is not targeted in hypertension because if blocked, individuals may suffer from orthostatic hypotension and fainting.

References

 

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