Heart rate and blood pressure relationship physiology

Orthostatic Blood Pressure and the Heart Rate

When we stand, the effect of gravity on the blood volume causes 500 to 800 mL of blood to pool in the lower extremities and splanchnic venous capacitance vessels of the abdomen6 (Fig. 99.2), reducing the venous return, stroke volume, and cardiac output. The reduction in stretch of the arterial and cardiopulmonary baroreceptors is sensed, and the reduced activity of the baroreceptor afferent nerves at their synapses in the NTS leads to a decrease in cardiac vagal tone and an increase in sympathetic activity. The release of norepinephrine causes both arterial vasoconstriction and venoconstriction and an increase in cardiac contractility and heart rate, and protects the arterial pressure and cerebral perfusion. To perform the orthostatic blood pressure test at the bedside, the patient should lie supine for 10 minutes before the baseline BP and HR are measured and recorded, and then should stand at the side of the bed. BP and HR measurements are repeated at 1 and 3 minutes, and at 5 minutes if possible, with the patient queried about symptoms each time. In young healthy persons, baroreflex compensation is so perfect that the systolic BP (SBP) at 1, 3, and 5 minutes of quiet standing is often unchanged, whereas the diastolic BP (DBP) pressure rises 5 to 10 mm Hg and the HR rises less than 10 beats/min. If beat-to-beat BP rather than sphygmomanometric BP is being assessed, as when a Finapres device is being used or an arterial line is in place, one will often see a transient fall (lasting only seconds) in both the SBP and DBP with standing before the compensatory mechanisms readjust the system. In older individuals, compensation is often not as rapid or as complete. Criteria for orthostatic hypotension (OH) are not met in either young or old adults unless there is a fall in SBP of more than 20 mm Hg, or of DBP of more than 10 mm Hg at 3 minutes of standing quietly.7 An abnormal rise in HR is more than 20 beats/min. A feature of severe autonomic disorders with OH can be a BP that is extremely posture dependent. Some patients may have marked supine hypertension, with an SBP at or above 200 mm Hg, a nearly normal SBP when seated, and an SBP that falls to less than 60 mm Hg within less than a minute of standing. The upright BP clearly cannot be documented by sphygmomanometry in these patients at the bedside. For safety reasons, in the absence of beat-to-beat BP monitoring or an available tilt table, one may resort to documenting the “standing time” (i.e., the number of seconds the patient can stand before typical symptoms of light-headedness occur and the patient sits). This time can be used to assess the response to medications or other therapeutic maneuvers.

It is important to realize that in the absence of autonomic disorders, significant OH and even syncope can still be seen, most commonly with volume depletion due to gastrointestinal fluid loss, hemorrhage, excessive sweating, fever, or disorders such as Addison disease (decreased or absent adrenal function, with glucocorticoid and mineralocorticoid insufficiency). OH, especially with prolonged standing, can also be seen with loss of muscle tone and reduced vascular responsiveness, as with prolonged bedrest; it also occurs in astronauts who have been exposed to microgravity during spaceflight. In these situations, the rise in HR with standing will be excessive but appropriate for the fall in BP, unlike the blunted or absent rise seen in sympathetic incompetence.

Heart Rate

Heart rate is a useful guide for exercise as a result of having a linear relationship to Vo2. Maximum heart rate is best determined by testing and decreases with age. It can be estimated either by the Karvonen equation or by the equation heart rate = 220 − age.70 Physical conditioning can alter the slope of the relationship of heart rate and Vo2 with improved conditioning lowering the slope (less heart rate increase for a given Vo2). A limitation to using heart rate can be the alteration of heart rate response in the setting of medications that alter vagal and sympathetic tone.13

462.2

Sinus Arrhythmias and Extrasystoles

Phasic sinus arrhythmia represents a normal physiologic variation in impulse discharges from the sinus node related to respirations. The heart rate slows during expiration and accelerates during inspiration. Occasionally, if the sinus rate becomes slow enough, anescape beat arises from the atrioventricular (AV) junction region (Fig. 462.1). Normal phasic sinus arrhythmia is caused by the activity of the parasympathetic nervous system and can be quite prominent in healthy children. It may mimic frequent premature contractions, but the relationship to the phases of respiration can be appreciated with careful auscultation. Drugs that increase vagal tone, such as digoxin, may exaggerate sinus arrhythmia; it is usually abolished by exercise. Other irregularities in sinus rhythm, especially bradycardia associated with periodic apnea, are common in premature infants.

Sinus bradycardia is a result of slow discharge of impulses from the sinus node, the heart's “natural pacemaker.” A sinus rate <90 beats/min in neonates and <60 beats/min in older children is considered sinus bradycardia. It is typically seen in well-trained athletes; in healthy individuals it generally has no significance. Sinus bradycardia may occur in systemic disease (hypothyroidism, anorexia nervosa), and it resolves when the disorder is under control. It may also be seen in association with conditions in which there is high vagal tone, such as gastrointestinal obstruction or intracranial processes. Low-birthweight infants display great variation in sinus rate. Sinus bradycardia is common in these infants, in conjunction with apnea, and may be associated with junctional escape beats; premature atrial contractions are also frequent. These rhythm changes, especially bradycardia, appear more often during sleep and are not associated with symptoms. Usually, no therapy is necessary.

Wandering atrial pacemaker is defined as an intermittent shift in the pacemaker of the heart from the sinus node to another part of the atrium (Fig. 462.2). It is not uncommon in childhood and usually represents a normal variant. It may also be seen in association with sinus bradycardia in which the shift in atrial focus is an escape phenomenon.

Extrasystoles are produced by the premature discharge of an ectopic focus that may be situated in the atrium, the AV junction, or the ventricle. Usually, isolated extrasystoles are of no clinical or prognostic significance. Under certain circumstances, however, premature beats may be caused by organic heart disease (inflammation, ischemia, fibrosis) or drug toxicity.

Premature atrial contractions orcomplexes (PACs) are common in childhood, usually in the absence of cardiac disease. Depending on the degree of prematurity of the beat (coupling interval) and the preceding R-R interval (cycle length), PACs may result in a normal, a prolonged (aberrancy), or an absent (blocked PAC) QRS complex. The last occurs when the premature impulse cannot conduct to the ventricle due to refractoriness of the AV node or distal conducting system (Fig. 462.3). Atrial extrasystoles must be distinguished from premature ventricular contractions. Careful scrutiny of the electrocardiogram (ECG) for a premature P wave preceding the QRS will show either a premature P wave superimposed on and deforming the preceding T wave or a P wave that is premature and has a different contour from that of the other sinus P waves. PACs usually reset the sinus node pacemaker, leading to an incomplete compensatory pause, but this feature is not regarded as a reliable means of differentiating atrial from ventricular premature complexes in children.

▪ EFFECT OF HEART RATE ON CARDIAC PERFORMANCE

Heart rate (HR) plays a major role in determining cardiac function for various reasons. HR affects preload by determining the length of time for ventricular filling. Because coronary and therefore myocardial blood supply occurs during diastole, HR directly affects subendocardial blood flow. If subendocardial flow is compromised with shorter diastolic filling, ischemia may result. A downward spiral ensues because the ischemic, less-compliant heart resists optimal ventricular filling and preload decreases. Increased HR is critical during exercise to increase CO and meet increased metabolic needs. HR changes as a result of ongoingmultifactorial development; the effect of HR on cardiac function is discussed further in this context.

Heart Rate and Pulse Rate Monitoring

The ability to estimate the heart rate quickly with a “finger on the pulse” is as important as this expression is common despite near-universal use of electronic devices for continuous monitoring. The electrocardiogram (ECG) is the most common heart rate monitoring method used in the operating room, even though any device measuring the period of the cardiac cycle will suffice. Accurate detection of the R wave and measurement of the interval from the peak of one QRS complex to the peak of the next on an ECG (R-R interval) serve as the basis from which digitally displayed values are derived and periodically updated (e.g., at 5- to 15-second intervals) (Fig. 36.1).2

The distinction between heart rate and pulse rate lies in the difference between electrical depolarization with systolic contraction of the heart (heart rate) and a detectable peripheral arterial pulsation (pulse rate). Pulse deficit describes the extent to which the pulse rate is less than the heart rate and may arise in conditions such as atrial fibrillation in which stroke volume is periodically compromised by a very short R-R interval to such an extent that no arterial pulse is detectable for that systolic ejection. Electrical-mechanical dissociation and pulseless electrical activity are extreme examples of pulse deficit in which cardiac contraction is completely unable to generate a palpable peripheral pulse. The heart rate is reported from the ECG trace and the pulse rate from the pulse oximeter plethysmograph or arterial blood pressure monitor. Considering both in monitoring and clinical evaluation improves accuracy and reduces measurement errors and false alarms.3

Heart rate

Heart rate (HR) increases alongside oxygen uptake during exercise to reach steady-state HR during constant workload sub-maximal exercise, and up to maximal HR (HRmax) in incremental maximal exercise. Cardiac output during exercise increases initially due to an increase in stroke volume and then, with increasing workload, further increase becomes dependent on HR. In healthy people maximal exercise is limited by HRmax, which can be estimated using the equation 220 – age. In trained subjects the stroke volume is increased, therefore allowing a greater cardiac output for a given HR. The linear relationship between HR and VO2 can be used to predict VO2max from incremental exercise without requiring the person to work up to maximum exercise intensity. By plotting HR vs. VO2 through a range of workloads the linear relationship can be extended to reach the predicted HRmax. The corresponding VO2max can then be estimated from the graph (Figure 1.6).

2.3.2 Heart rate

Heart rate was recorded at 1 Hz during all exercise bouts and basketball free throws. Average heart rate in the 3 s prior to each basketball shot was calculated before these were averaged for each set of 10 pre- and post-intervention free throw basketball shots, within each condition, and for each participant (HR). The percentage of heart rate maximum (%HRM) during each set of 10 pre- and post-intervention basketball free throws, within each condition, was deduced using the maximum heart rate recorded at exhaustion during the maximal ramp incremental exercise test or the severe-intensity exercise bout.

2 Heart Rate

Heart rate is measured from the ECG signal. A heart rate of 180 to 200 beats/min correlates with maximal oxygen consumption in both boys and girls. Therefore, an effort is made to encourage all children to exercise to attain this heart rate. The mean maximal heart rates for all subjects were virtually identical, 198 ± 11 beats/min for boys and 200 ± 9 beats/min for girls. Heart rate declined abruptly during the first minute of recovery to 146 ± 19 beats/min for boys and 157 ± 19 beats/min for girls.

Inadequate increments in heart rate may be seen with sinus node dysfunction, in congenital heart block, and after cardiac surgery. Sinus node dysfunction is common after surgery involving extensive atrial suture lines, such as the Senning operation or Fontan operation. It is also common after repair of TOF. Marked chronotropic impairment significantly decreases aerobic capacity. Trained athletes tend to have lower heart rates at each exercise level. An extremely high heart rate at low levels of work may indicate physical deconditioning or marginal circulatory compensation.

Heart Rate

Heart rate is an important physiologic regulator of total cardiac output. Through strong influences of the autonomic nervous system, the heart rates in a newborn can range from 70 to 220 beats/min and profoundly impact cardiac output. Coordinated electric activity and automaticity of the conduction system in the newborn heart are essential to maximizing the active phase of ventricular filling. Overall, the relationship between heart rate and total cardiac output is complex.

The most important influences on the automaticity of the SA node come from the sympathetic and parasympathetic divisions of the autonomic nervous system. Fibers from these two divisions alter the intrinsic heart rate by changing the course of spontaneous diastolic depolarization on pacemaker cells in the SA node. Activation of the cardiac sympathetic fibers will increase the heart rate, whereas stimulation of cardiac parasympathetic fibers will decrease the heart rate. These neural influences have immediate effects and can therefore cause very rapid adjustments in cardiac output.

However, the effect of changes in heart rate on cardiac output is complex, and the relationship is not linear. This is because a change in heart rate can alter the three determinants (preload, afterload, and contractility) of SV. A significant increase in heart rate would decrease the duration of diastole and diminish ventricular filling, thereby reducing preload.126 On the other hand, this rise in heart rate would also increase the net rate of calcium influx into the cardiomyocyte, enhancing contractility. This effect of heart rate on cardiac output has been verified in many types of experimental studies in animals and humans (Fig. 13.10).127-130

This characteristic relationship between cardiac output and heart rate is critically important in the postsurgical care of patients with congenital heart disease with excessively slow or fast heart rates. For example, complete heart block from procedures involving the closure of a ventricular septal defect can result in a profound decrease in cardiac output because the compensatory increase in SV is insufficient to offset the very slow heart rate and lack of atrioventricular synchrony.131 Medication with the potential to slow heart rate should be used cautiously in the postoperative setting to minimize risk of lowering cardiac output. At the other extreme, JET is common postoperatively in infants and requires emergency treatment because cardiac output might be significantly compromised due to decreased diastolic filling time resulting from excessively rapid heart rates and lack of atrioventricular synchrony.132,133

Heart Rate

The maximum heart rate achievable at peak exercise tends to decline with age. For treadmill exercise, the normal peak heart rate is commonly estimated from the equation:

PeakHR=220-age(inyears)36

Peak heart rate on a bicycle tends to be about 5% to 10% less than on a treadmill.37

Normally, during a progressive exercise test, heart rate rises linearly in proportion to