What’s in a blood pressure reading?
What do the numbers actually mean?
Blood pressure readings in clinical practice are normally derived from the large arteries such as brachial (usually used in non-invasive BP monitoring) or radial and femoral (commonly used in arterial line monitoring).
Systolic and diastolic blood pressure
The systolic blood pressure (SBP) represents the peak pressure experienced in the arterial system as a result of ventricular contraction. SBP is primarily affected by the stroke volume (SV; ie the amount of blood ejected from the heart) and how compliant the aorta and large arteries are (a high compliance buffers blood pressure and reduces SBP, whilst low compliance results in higher arterial wall stress and higher SBP).
The diastolic blood pressure (DBP) is the minimum pressure in the arterial system, determined by the pressure within the arteries whilst the ventricles are filling before the next contraction. This is affected by the heart rate (a slower heart rate allows more blood to leave the arterial system each cycle, giving a lower DBP), systemic vascular resistance (a higher degree of arterial tone reduces blood runoff and increases DBP), and arterial compliance (stiff, poorly compliant arteries don’t recoil as much, reducing the arterial wall pressure during diastole and, thus reducing DBP). Diastole is also the time during which the left coronary circulation is perfusing the left side of the heart.
SBP is reflective of stroke volume (SV) and arterial compliance.
DBP is reflective of systemic vascular resistance (SVR) and arterial compliance.
Of these variables, arterial compliance is generally much less acutely changeable. Thus, it can be useful to consider SBP as a proxy for SV, whilst DBP can give an indication of SVR. Whilst the caveat is that physiology fiendishly resists such simplification, this heuristic has utility in interpreting SBP and DBP at the bedside.
Pulse Pressure
The pulse pressure (PP) is the amplitude of the arterial pressure wave, or the delta between these two extreme ends of the arterial pressure. It provides a sense of stroke volume, arterial compliance, and systemic vascular resistance. A widened pulse pressure can be caused by a raised SBP, a reduced DBP, or both. A narrowed blood pressure can be caused by a reduced SBP, a raised DBP or both.
In the case of a widened pulse pressure, SV, SVR and arterial compliance all contribute in different ways.
- Increased stroke volume results in more blood ejected into the arterial circulation, causing a higher pressure on the vessel walls and higher SBP.
- Similarly, reduced arterial compliance means that the vessels’ ability to accommodate blood volume is reduced, with stroke volume transmitting higher pressures to the vessel walls and raising SBP. Due to the lack of recoil (see windkessel effect below), the DBP may also be reduced, further widening the pulse pressure. On the contrary, a normal or higher arterial compliance won’t necessarily cause a lower SBP, it will likely just prevent an exaggerated SBP.
- A reduced SVR, such as in sepsis causing inappropriate vasodilation, lowers the pressure on the vessel and reduces DBP.
The opposite cause and effects hold true in the case of a narrowed PP.
As previously mentioned, arterial compliance will affect SBP (and consequently PP), but it will not markedly fluctuate in the acute setting. So whilst stiff arteries may give a higher baseline SBP in a patient, we can infer changes in stroke volume and systemic vascular resistance by tracking fluctuations in the pulse pressure within an acute patient encounter.
In this sense, whilst it is important to acknowledge the effect of arterial compliance on pulse pressure, we can predominantly focus on its utility to gauge SV and SVR.
Factors that may increase PP:
- ↑ SV → ↑ SBP
- ↓ arterial compliance → ↓ dampening of SBP → ↑ SBP
- ↓ SVR → ↓ DBP
Factors that may narrow PP:
- ↓ SV → ↓ SBP
- ↑ arterial compliance → ↑ dampening of SBP → may cause ↓ SBP
- ↑ SVR → ↑ DBP
Like everything in medicine, the clinical context is key in determining what causes a specific pulse pressure.
An example blood pressure of 90/70 mmHg gives a pulse pressure of 20 mmhg; a narrow PP.
The SBP of 90 mmHg suggests that stroke volume is low, whilst the DBP is preserved at 70 mmHg, likely reflecting a reasonable SVR. If this was a trauma patient, we might deduce that they have a low circulating volume due to hemorrhagic shock, causing a low stroke volume, with a compensatory sympathetic drive to maintain SVR.
On the other hand, if this were a heart failure patient, this may represent poor stroke volume due to cardiac failure, with a normal DBP due to congestion and/or sympathetic drive increasing SVR. The first patient likely needs to be given volume resuscitation, the second may need diuresis.
Consider how aortic stenosis or regurgitation may affect pulse pressure.
Aortic stenosis increases afterload of the left ventricle, reducing effective stroke volume. This would likely reduce SBP, and with DBP usually unaffected, this usually results in a narrowed pulse pressure.
Aortic regurgitation causes back flow of blood from the aorta back into the left ventricle during diastole. This results in lower DBP and, often, a compensatory increased contractility/stroke volume which raises SBP. The sum of this is a widened pulse pressure
An important difference between arterial compliance and SVR
Both arterial compliance and SVR describe processes within the arterial system that affect blood pressure, but they refer to different arterial zones and physiologies.
The influence of arterial compliance on SBP is predominantly derived from the aorta and large arteries, which is where blood leaving the left ventricle immediately enters. Arterial compliance describes the change in cross-sectional area for a given pressure in an artery; the greater the stretch, the higher the compliance. This stretch is a passive quality of the arteries that stores energy after systole, recoiling to maintain forward blood flow during diastole (the Windkessel effect). Compliance of the arteries is greatest proximally (the aorta being the most compliant), becoming increasingly stiffer more peripherally due to higher smooth muscle density (eg radial and dorasalis pedis arteries being much stiffer and less compliant than the aorta.).
SVR, however, is determined by the much smaller arterioles, and represents a more active and variable modulator of blood pressure. Arteriolar radius, being just prior to the capillaries and where perfusion occurs, is adjusted by local mechanisms for the purposes of maintaining perfusion. This affects the rate of emptying from the arteries and run-off into the capillaries, thereby altering DBP. Arteriolar radius can be actively and rapidly adjusted to alter regional blood flow and, subsequently, SVR.
The Windkessel effect
As stated, the walls of large arteries are elastic and distend to accommodate blood ejected from the left ventricle, which helps to buffer rises in blood pressure. After systole, the elastic recoil of these arteries drives the blood onward through the circulation, maintaining diastolic pressure and continuous onward blood flow throughout the cardiac cycle.
This windkessel mechanism relies on adequate compliance of the arteries, something which reduces with age, hypertension, atherosclerosis and chronic inflammatory states. Without this arterial compliance, blood flow would be markedly reduced in between each ventricular contraction during diastole, affecting downstream tissue perfusion.
Summary:
SBP reflects the force and volume of ventricular contraction (stroke volume), as well as the arterial compliance of the aorta and large vessels against which the heart must contract.
DBP reflects the systemic vascular resistance (high SVR = ↑ DBP) and is also influenced by heart rate (slow HR = longer runoff time = ↓ DBP).
Pulse pressure is the difference between SBP and DBP, and helps to further inform our impression of stroke volume, arterial compliance and systemic vascular resistance.