Blood Pressure and Heart Rate Variability

By Geoffrey A Head Baker IDI Heart and Diabetes Institute,  9 May 2012

  

Blood pressure (BP) is most commonly thought of as the reading taken at the GP clinic consisting of a single set of 2 numbers such as 120/80 being “normal”.  However, BP is highly variable depending on your situation, activity and time of day. BP and pulse rate are highest during the day and goes down considerably during sleep. Emotional stress, exercise and even waking up can cause marked increases in your BP. While these changes are considered to be normal as part of our daily lives, they are not necessarily without some risk particularly for the elderly or those with other cardiovascular risk factors such as hypertension, diabetes. Patients with hypertension have more variable BP and less variable pulse rates and that this in itself (independent of the hypertension) is an added cardiovascular risk factor. It has recently been found  that an excessive BP rise during exercise can occur in some people and this is associated with masked hypertension and cardiac hypertrophy (Sharman et al., 2011).   

Role of ambulatory BP monitoring(ABPM)

ABPM provides a set of readings of BP and pulse rate a period of usually not less than 24 hours. Thus BP is measured during sleep and during a normal active day. ABPM gives a much better indication of the overall BP of a person and is considered to be much more accurate than single clinic measures of BP. The process also avoids much of the reaction of patient to having the BP measured by the doctor which is known as the “white coat” effect. Importantly, ABPM provides information on Short-term BP and HR variability (measured as standard deviation for daytime readings or night-time readings), diurnal BP and HR variability (day–night difference) as well as long-term BP and HR variability (when ABP monitoring repeated 6-monthly or yearly).

BP variability is an important measure and should be taken into account when examining ABPM reports from patients. High levels of BP variability at night time and daytime relates to a higher risk of end-organ damage(Parati, 2005). Daytime systolic BP variability has been correlated with CVD mortality risk (Kikuya et al., 2000).

Low levels of pulse rate variability which can occur in patients with hypertension and also type II diabetes can indicate dysfunction of the nervous system to the heart. Such a condition in itself is an important cardiovascular risk factor.  

Morning BP surge

The morning waking period is a particularly “risky time” as the risk of stroke, sudden cardiac death or myocardial infarction is 2-4 times higher in the morning (Willich et al., 1987) . At this time there is usually increases in BP, heart rate, circulating catecholamines, other hormones and blood tendencies to clot more readily (Weber, 2002). The size and the rapidity of the morning BP surge is exaggerated in patients with hypertension (Head and Lukoshkova, 2008). Morning systolic BP measured by ABP monitoring is a strong independent predictor of stroke and other CVD outcomes (Li et al., 2010, Kario et al., 2006). Morning BP can also be measured using home BP measurement (Stergiou and Parati, 2009, Redon et al., 2001). In older patients with hypertension, morning BP surge (difference between morning BP and nadir during sleep) measured by ABP monitoring is strongly correlated with the risk of stroke, independent of mean BP and nocturnal BP (Kario et al., 2003). 

Long term BP variability

When blood pressure varies considerably over a weeks to months this can only by frequent repeated assessments. If the periods of higher BP are sufficient, this can be classed as “periodic hypertension”. For patients receiving treatment for high BP, such long-term (between-visit) clinic systolic BP variability and maximum daytime ambulatory systolic BP are predictors of stroke risk, independent of mean systolic BP (Rothwell et al., 2010b, Rothwell et al., 2010a). 

  

  

Bibliiography

  

Head, G. A. and Lukoshkova, E. V. (2008) Clin Exp Pharmacol Physiol, 35, 516-521.

Kario, K., Ishikawa, J., Pickering, T. G., Hoshide, S., Eguchi, K., Morinari, M., Hoshide, Y., Kuroda, T. and Shimada, K. (2006) Hypertens Res, 29, 581-7.

Kario, K., Shimada, K. and Pickering, T. G. (2003) J Cardiovasc Pharmacol, 41 Suppl 1, S61-6.

Kikuya, M., Hozawa, A., Ohokubo, T., Tsuji, I., Michimata, M., Matsubara, M., Ota, M., Nagai, K., Araki, T., Satoh, H., Ito, S., Hisamichi, S. and Imai, Y. (2000) Hypertension, 36, 901-6.

Li, Y., Thijs, L., Hansen, T. W., Kikuya, M., Boggia, J., Richart, T., Metoki, H., Ohkubo, T., Torp-Pedersen, C., Kuznetsova, T., Stolarz-Skrzypek, K., Tikhonoff, V., Malyutina, S., Casiglia, E., Nikitin, Y., Sandoya, E., Kawecka-Jaszcz, K., Ibsen, H., Imai, Y., Wang, J. and Staessen, J. A. (2010) Hypertension, 55, 1040-8.

Parati, G. (2005) J Hypertens Suppl, 23, S19-25.

Redon, J., Bertolin, V., Giner, V. and Lurbe, E. (2001) Blood Press Monit, 6, 207-210.

Rothwell, P. M., Howard, S. C., Dolan, E., O'Brien, E., Dobson, J. E., Dahlof, B., Poulter, N. R. and Sever, P. S. (2010a) Lancet Neurol, 9, 469-80.

Rothwell, P. M., Howard, S. C., Dolan, E., O'Brien, E., Dobson, J. E., Dahlof, B., Sever, P. S. and Poulter, N. R. (2010b) Lancet, 375, 895-905.

Sharman, J. E., Hare, J. L., Thomas, S., Davies, J. E., Leano, R., Jenkins, C. and Marwick, T. H. (2011) Am J Hypertens, 24, 898-903.

Stergiou, G. and Parati, G. (2009) J Hypertens, 27, 696-9.

Weber, M. A. (2002) Am J Cardiol, 89, 27A-33A.

Willich, S. N., Levy, D., Rocco, M. B., Tofler, G. H., Stone, P. H. and Muller, J. E. (1987) Am J Cardiol, 60, 801-806.

  

  

  

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