Physiology review: Circulatory system

Chances are you frequently care for patients with cardiac and circulatory conditions and administer drugs affecting the circulation. This review of the circulatory system increases your knowledge base so you can more efficiently assess patients with signs and symptoms of cardiovascular problems.

The circulatory system includes the heart, blood vessels, and regulatory controls (such as the autonomic nervous system, catecholamines, and hormones). Its main function is to deliver oxygen and substrate (glucose) to cells. The circulatory system also transports byproducts of cellular metabolism—66% in the form of carbon dioxide (CO2) to the lungs and the remaining 33% to the kidneys as breakdown products of protein metabolism. Metabolism of oxygen and glucose (cellular combustion) produces heat, which is conducted through the circulation and warms the body.

In a healthy person, circulatory system components function effectively. But when one of the components or regulatory mechanisms malfunctions, the circulatory process and its secondary mechanisms are compromised. Because the heart is a volumetric pump, intravascular volume is a key functional component, controlled by the kidneys and various neurohormonal factors. (See the box below.)


Neurohormonal regulation of circulation

Cellular demands regulate cardiac output (CO) through an intricate system of vascular autoregulation, neuroregulation, and hormonal control. This regulatory system controls blood flow to individual organs and can affect the heart directly.

For example, endogenous catecholamines are secreted during hemorrhage to maintain perfusion to vital organs (brain, heart, and kidneys). Catecholamines also affect the heart rate to maintain CO in the face of decreasing stroke volume (SV). This compensatory mechanism increases the volume of blood ejected into the aorta. When the heart rate exceeds 150 beats/minute, atrial and ventricular filling decrease (decreased preload), further reducing SV beyond the ability to compensate. As a result, CO declines.

Besides causing arterial constriction, endogenous or exogenous catecholamines increase venous tone, which reduces venous compliance and increases the amount of blood volume that contributes to the pressure; driving blood back to the heart to maintain mean systemic pressure. Catecholamines also heighten the heart’s inotropic state, causing contractility to increase, which in turn improves cardiac performance. These mechanisms allow the circulatory system to adapt to various activities and to compensate during disease states.


Cardiac output, blood pressure, resistance, and impedance

Heart function can be described in terms of cardiac output (CO), or the output of blood circulating through the body over 1 minute. Normally, CO ranges from 5 to 8 L/minute.

Continuous blood circulation requires an alternating pressure differential—namely, blood pressure (BP). BP drives blood through the circulatory system due to interaction between a pressure-generating source (the heart) and the circulatory system, which creates a closed circuit (blood vessels). On the arterial side, this blood circuit is called systemic vascular resistance (SVR), a calculation used to approximate resistance within the arterial circuit. BP equals CO multiplied by SVR. (BP = CO x SVR.)

However, the circulation functions more through impedance, as a deformable tube would, rather than resistance, as a rigid tube would. That’s because the aorta resembles a tube that offers both resistance and compliance as blood ejects from the heart. For example, a young person may safely increase her CO to 20 L/minute during exercise because she has adequate aortic compliance. An elderly person with a calcified aorta may not tolerate this dramatic CO increase because of decreased aortic compliance, which raises resistance and elevates BP significantly.

Heart rate, stroke volume, and ejection fraction

CO can be further divided into its key components—heart rate (HR) and stroke volume (SV). SV refers to the difference between end-diastolic volume (EDV, left ventricular blood volume before contraction) and end-systolic volume (left ventricular volume at the end of contraction). For example, EDV of 120 mL divided by an end-systolic volume of 50 mL equals an SV of 70 mL.

CO equals HR times SV. (CO = HR x SV). Normal SV ranges from 50 to 80 mL; for an average adult, it’s typically 70 mL.

The percentage of blood ejected from the ventricles is called the ejection fraction (EF). EF equals SV divided by EDV. (EF = SV ÷ EDV.) In the previous example, during the diastolic phase the ventricle refills to a capacity of 120 mL. During the next (systolic) phase, the left ventricle contracts and displaces an SV of 70 mL into the aorta. So in this example, EF is 58%. (SV÷ EDV, or 70 ÷ 120.)

Determinants of stroke volume

Factors that determine SV are cardiac contractility, preload, afterload, heart rate, and heart rhythm. Contractility refers to the ability of the atria or ventricle to contract, with the primary purpose to eject or displace blood into the ventricle or aorta respectively; this is commonly called the heart’s inotropic state. Assessed by palpating the pulses, contractility is affected by drugs (inotropes) and volume states (euvolemia, hypervolemia and hypovolemia). A fast pulse doesn’t necessarily imply optimal contractility. An increased pulse reduces the time allowed for the atria and ventricles to fill, which decreases preload.

Preload and afterload

Preload refers to the blood volume of a heart chamber. A stretching force applied to the cardiac muscle, it determines precontraction muscle length. The degree of interlocking between cardiac muscle fibers increases as stretch increases, which in turn heightens preload. In turn, this strengthens contraction (Frank-Starling relationship). In other words, the greater the stretch, the greater the contractile force.

Venous return is determined by mean systemic pressure (Pms)—pressure remaining in the circulation during asystole, which drives blood back to the heart. Right atrial pressure (RAP) or central venous pressure (CVP) refers to the pressure that impedes blood return. Venous return equals Pms minus RAP. The greater the difference between Pms and RAP, the greater the venous return and preload.

For example, during spontaneous inspiration, RAP drops (because thoracic pressure decreases) and pressure in the abdomen rises, thereby increasing venous return. As preload stretches cardiac muscle fibers, the heart’s contractility increases until the point of overstretching. Therefore, as venous return rises during the diastolic phase, the ventricle fills and increased preload stretches the heart muscle in preparation for generating the pressure needed for systolic contraction.

Afterload refers to the tension or stored energy that must develop in a cardiac muscle fiber before shortening (systolic contraction) can take place. The resultant force (pressure) developed during systolic contraction must exceed the opposing force in the aorta and arterioles for blood to be ejected into the arterial tree. The main impedance to blood ejected from the ventricle is generated in the aorta and the pressure within it by arterioles. Therefore, afterload rises with systemic hypertension as the ventricles must generate greater pressure to overcome the impedance of increased systemic pressures.

Transport system

The circulatory transport system resembles an enormous branching tree; if combined end to end, the various branches would measure roughly 30,000 miles of blood vessels. The heart is the engine of the transport system. As the heart’s energy or pressure is displaced into the circulatory system, pressure falls progressively along a gradient. On the arterial side, pressure is highest in the larger vessels (arteries) and decreases throughout the system, reaching its lowest point in the smaller vessels (capillaries).

In addition, as blood travels further from the aorta where the circulatory tree divides, resistance to blood flow decreases as cross-sectional area increases. Although the volume pumped out of the heart equals the volume that returns to the heart (CO = venous return), total blood volume isn’t distributed equally within the circulatory system. Most of the total blood volume is stored on the venous side as a reservoir. As the heart ejects blood and blood flows down the circulatory tree into the venous reservoir, a second or passive peripheral pump drives blood back to the heart, with Pms driving venous return. The peripheral circulation controls Pms and drives blood back to the right atrium.

For example, a large blood volume remains in the liver and spleen as a reserve. As we breathe and create a negative pressure, the diaphragm contracts and descends from the thoracic compartment into the abdominal cavity. This contraction raises intrabdominal pressure, driving blood from the reservoir in the liver and spleen back to the heart.

Simultaneously, thoracic pressure decreases with inspiration and reduces RAP, increasing the pressure gradient to the heart. The greater the gradient between Pms and RAP, the greater the venous return and CO.

Dynamic interactions

The dynamic interactions between the heart and tissue requirements allow the body to function through a spectrum of activities—or to compensate in disease states. The heart serves primarily to deliver oxygen and glucose to the body. Its function is affected by both preload and afterload, and adjusts dynamically over a range of activities to deliver nutrients and oxygen to keep the organs functioning properly. Hospital patients may have altered cardiac function due to such conditions as pain, fear, agitation, or infection. As a nurse, you must be able to recognize states of altered cardiac function so you can provide optimal care.

The authors work at R Adams Cowley Shock Trauma Center in Baltimore, Maryland Penny Andrews is a staff nurse. Nader M. Habashi is an intensivist and multitrauma critical care medical director.

Selected references

Guyton AC, Lindsey AW, Kaufmann BN. Effect of mean circulatory filling pressure and other peripheral circulatory factors on cardiac output. Am J Physiol. 1955;180: 463-8.

Mikkelsen ME, Miltiades AN, GaieskiF D, et al. Serum lactate is associated with mortality in severe sepsis independent of organ failure and shock. Crit Care Med. 2009 May;37(5):1670-7.

Klabunde RE. Cardiovascular Physiology Concepts. (2nd ed.). Lippincott Williams & Wilkins; 2011.
Tuggle D. Hypotension and shock: the truth about blood pressure. Nursing. Fall 2010;40:Ed Insider:1-5.

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