1 Foundations of Hemodynamics

Pressure, flow, and resistance

Hemodynamics connects three basic ideas: pressure describes force, flow describes blood moved over time, and resistance describes opposition to that flow. Blood moves through the circulation because of pressure gradients, proceeding from higher pressure toward lower pressure.

A general relationship is:

A larger pressure difference increases flow, while greater resistance reduces it. Resistance is strongly affected by vessel radius: narrowing small arteries and arterioles raises resistance, and widening them lowers it. Because radius has a large effect, modest changes in vessel diameter can substantially alter blood flow and pressure.

The two circulations

The heart drives blood through two connected loops. In the pulmonary circulation, the right ventricle pumps blood through the lungs, where it takes up oxygen, and the blood returns to the left side of the heart. This circuit is normally lower in pressure and resistance.

In the systemic circulation, the left ventricle pumps blood to the body’s tissues, and blood returns through the veins to the right side of the heart. This is normally a higher-pressure circuit. In a steady state, the right and left ventricles pump approximately the same volume of blood over time.

Understanding blood pressure

Blood pressure is commonly recorded as systolic pressure over diastolic pressure. Systolic blood pressure (SBP) is arterial pressure during ventricular contraction; diastolic blood pressure (DBP) is arterial pressure during ventricular relaxation.

Pulse pressure is the difference between systolic and diastolic pressure:

Mean arterial pressure (MAP) is the average arterial pressure over one cardiac cycle. At a typical heart rate, it can be estimated as:

This estimate is less reliable when heart rate or the duration of systole is unusual. Blood pressure reflects both cardiac output and systemic vascular resistance, so a pressure reading alone does not reveal the entire hemodynamic picture. Similar pressures can result from different combinations of flow and resistance.

Cardiac output and stroke volume

Cardiac output (CO) is the volume of blood pumped by a ventricle per minute. It is calculated from heart rate and stroke volume:

Stroke volume (SV) is the amount ejected in one beat. It is calculated as end-diastolic volume minus end-systolic volume:

For example, a heart rate of $70$ beats per minute and a stroke volume of $70$ millilitres per beat produce a cardiac output of $4{,}900$ millilitres per minute, or $4.9\ \mathrm{L/min}$. Cardiac output can change when heart rate or stroke volume changes. A faster heart rate does not always increase output: a very fast rate may reduce ventricular filling time and stroke volume.

Relating pressure to cardiac output

Systemic circulation can be described approximately by relating cardiac output to mean arterial pressure, central venous pressure, and systemic vascular resistance:

When central venous pressure is small relative to mean arterial pressure, this is often simplified to:

These are approximations. Actual flow depends on a pressure difference, and cardiovascular measurements are affected by factors such as arterial elasticity and pulsatile flow.

The relationship also shows why blood pressure alone does not determine cardiac output. Two people with the same mean arterial pressure could have different combinations of cardiac output and vascular resistance: one could have relatively high output and lower resistance, while another has lower output and higher resistance.

Factors that influence stroke volume

Three major influences on stroke volume are preload, contractility, and afterload. They describe different aspects of ventricular function and should be interpreted together.

Preload describes ventricular muscle stretch at the end of filling, or end diastole. It is related to ventricular filling and venous return. Within the heart’s functional range, increased filling can stretch cardiac muscle fibers and produce a stronger contraction, increasing stroke volume. This is the Frank–Starling mechanism. The effect is not unlimited: excessive filling does not necessarily improve output.

Preload is a physiological state rather than a single pressure reading. Filling pressures can serve as indirect estimates, but they do not always correspond closely to ventricular volume or muscle stretch.

Contractility is the strength of myocardial contraction at a given preload and afterload. Greater contractility can increase the volume ejected per beat, while impaired contractility can reduce stroke volume and cardiac output.

Afterload is the load a ventricle must overcome to eject blood. For the left ventricle, it is influenced by arterial pressure and systemic vascular resistance. For the right ventricle, it is influenced by pressure and resistance in the pulmonary circulation. Increased afterload can make ejection more difficult and reduce stroke volume, particularly when the ventricle is weak. Afterload is broader than any one pressure or resistance measurement.

Interpreting hemodynamic variables together

A change in preload may change stroke volume, which changes cardiac output and can in turn affect arterial pressure. Likewise, identical blood pressures can arise from different underlying combinations of flow and resistance.

Interpret hemodynamic variables together: pressure describes force, flow describes blood moved over time, and resistance describes opposition to that flow. Their equations provide a framework for understanding relationships, but they do not replace assessment of the whole cardiovascular picture.