Variations in Blood Pressure

Describe the physiological factors that may contribute to pulse variations in blood pressure

Blood pressure is not uniform throughout the circulation. Ventricular ejection generates two waves:

  • A blood flow wave
    Travels at ~20cm.s-1.
  • An arterial pressure wave
    Distends the elastic walls of the large arteries during systole, which then recoil during diastole to facilitate continual blood flow. This is the Windkessel effect.
    • This wave travels at 4m.s-1
    • This is what is felt when pulses are palpated, and what is seen on the arterial line waveform

Key pressures measured are:

  • Systolic blood pressure
    Maximal pressure generated during ejection.
    • Determined by:
      • Stroke volume
      • Systolic time
      • Arterial compliance
      • Reflected pressure wave
    • Relevant for:
      • Bleeding
        • Clot disruption
        • Aneurysmal wall pressure
  • Diastolic pressure
    Pressure exerted by the circulation upon the aortic valve.
    • Determined by:
      • Circulatory compliance
      • Circulating volume
      • Aortic valve (in)competence
    • Relevant for:
      • Coronary perfusion
  • Mean arterial pressure
    Average pressure in the circulation throughout the cardiac cycle, as measured by the area under the curve of the arterial line waveform.
    • Determined by:
      • Systolic blood pressure
      • Diastolic blood pressure
      • Heart rate
        Increasing HR will tend to increase MAP, as overall systolic time (and therefore time spent at higher pressure) is increased.
      • Shape of the arterial waveform/diastolic runoff
        The slow decrease in pressure after peak systolic pressure represent elastic recoil of large arteries, increasing the pressure driving blood into the peripheral circulation. A longer diastolic runoff period leads to a larger area under the curve, and a higher MAP.
    • Relevant for:
      • Organ perfusion

Changes by Site of Measurement

Measured pressure changes predictably at more distal sites:

  • All gradients are increased
    Arterial upstroke and falloff are both steeper.
  • The SBP increases
  • DBP decreases
  • MAP is constant
  • The dicrotic notch occurs later and becomes less sharp
    This occurs due to reflections in arterial pressure waves.

Respiratory Variation

Ventilation causes variation in peak systolic pressure due to dynamic changes in cardiac loading conditions:

  • Negative pressure respiration (i.e. regular breathing) generates a negative intrathoracic pressure during inspiration
    • Augments right ventricular function
      • Increased VR
        Via negative intrathoracic pressure.
      • Increases RVEDV
        RV moves up the Starling curve.
    • Impedes left ventricular function
      • Pooling of blood in the pulmonary circulation
      • Decreased LVEDV
        LV filling restricted by increased RV EDV; this is an example of intraventricular interdependence.
      • Increased afterload
        Negative intrathoracic pressure increases LV transmural pressure, increasing wall tension, and therefore afterload.
      • Decrease in SV and SBP
  • Positive pressure ventilation causes generally opposite effects Increased intrathoracic pressure during inspiration:
    • Decreases VR but increases LV filling via compression of the pulmonary circulation
    • Note that LV afterload is reduced throughout the respiratory cycle with the application of PEEP
  • When this change is >10mmHg, it is known as pulsus paradoxus
  • The magnitude of this effect varies with:
    • Magnitude of intrathoracic pressure change
      Large changes in intrathoracic pressure cause correspondingly larger changes in ventricular filling.
    • Other factors affecting cardiovascular function
      • Preload
        • Volume state
      • Compliance
        • Pericardial compliance
          • Constriction
          • Tamponade
        • Cardiac compliance
          • Diastolic dysfunction
      • Afterload
        • PE
        • Raised intrathoracic pressure
  • These differences can be measured:
    • Qualitatively
      By looking at respiratory swing on an arterial line or plethysmograph; or by palpation.
    • Quantitatively
      Using pulse pressure or stroke volume variation.

Pulse Pressure Variation

Describes the variation in pulse pressure over the course of a respiratory cycle. Pulse pressure variation is:

  • Mathematically defined as:
    • Therefore, it is calculated as a percent
  • Used as an indicator of fluid responsiveness
    • Patients higher on the Frank-Starling curve will have less change in stroke volume with an increase in preload, and therefore:
      • Reduced PPV
      • Be less fluid responsive
    • A PPV of >12% suggests volume responsiveness.
    • Note that this does not necessarily mean a fluid responsive patient needs fluid.
  • Reliant on several assumptions:
    • Regular sinus rhythm
      Irregular heart rates (particularly AF) lead to significant alterations in ventricular filling and therefore pulse pressure, independent of the respiratory cycle.
    • Controlled mechanical ventilation
      No spontaneous efforts.
    • Adequate tidal volumes
      Must be >
    • Normal chest wall compliance
      Requires a closed chest.

Stroke Volume Variation

SVV is:

  • Alternately defined as:
    • The percent change in stroke volume during inspiration and expiration over the previous 20 seconds
    • Variation of beat-to-beat SV from the mean value over the previous 20 seconds
  • Calculated by specialised devices from an invasive arterial waveform
    Calculation incorporates:
    • Pulse pressure
    • Vascular compliance
      Estimated from nomograms based on patient age, gender, height, and weight.
    • Vascular resistance
      Estimated from arterial waveform shape.
  • An alternative to PPV in measuring fluid responsiveness
    Relies on similar principles.
  • Probably less specific but more sensitive than PPV for identifying fluid responders

Circulatory Factors

Changes in circulatory function:

  • Inotropy
    The rate of systolic upstroke is related to , and therefore contractility.
  • SVR
    The gradient between the peak systolic pressure and the dicrotic notch gives an indication of SVR. E.g., a steep downstroke suggests a low SVR, as the pressure in the circulation rapidly falls when ejection ceases.
  • Preload
    A beat-to-beat variation is seen with the respiratory cycle, due to the change in preload occurring with changes in intrathoracic pressure.

Pathological Changes

Some pathological causes include:

  • Aortic Stenosis
    Causes a reduction in:
    • Pulse pressure
      Due to reduced stroke volume.
    • Gradient of upstroke
      Due to reduced stroke volume.
  • Aortic Regurgitation
    • Wide pulse pressure
      Combination of:
      • Increased SBP due to the increased force of ejection due to increased preload (Starlings Law), which occurs due to high ESV
      • Decreased DBP due to part of the stroke volume flowing back into the ventricle through the incompetent valve


  1. Chambers D, Huang C, Matthews G. Basic Physiology for Anaesthetists. Cambridge University Press. 2015.
  2. Buteler, Benjamin S. The relation of systolic upstroke time and pulse pressure in aortic stenosis. British Heart Journal. 1962.
  3. Mark, Jonathan B. Atlas of cardiovascular monitoring. New York; Edinburgh: Churchill Livingstone, 1998.
  4. Marik PE. Techniques for assessment of intravascular volume in critically ill patients. J Intensive Care Med. 2009;24(5):329-37.
  5. Soliman RA, Samir S, el Naggar A, El Dehely K. Stroke volume variation compared with pulse pressure variation and cardiac index changes for prediction of fluid responsiveness in mechanically ventilated patients. Egypt J Crit Care Med. 2015;3(1):9-16. doi:10.1016/J.EJCCM.2015.02.002
Last updated 2021-08-23

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