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Control of Cardiac Output

Page history last edited by PBworks 14 years, 5 months ago

Control of Cardiac Output (Chapter 24)

 

Objectives

  • Describe the principal determinants of cardiac output
  • Describe the principal determinants of cardiac preload and afterload
  • Explain the mechanical coupling between the heart and blood vessels
  • Explain the principals used in measuring cardiac output

 

  • The heart as a "demand" pump.

Cardiac output must be varied over a wide range to supply blood for tissues that may be resting, exercising, secreting, metabolizing, transporting, etc. From a resting output of 5 l/min, cardiac output can be increased to 20 l/min depending on the body’s demand for O2. The means available to vary cardiac output include heart rate, which can vary from 45 bpm in trained athletes (70 bpm in the rest of us) at rest, up to 200 bpm during strenuous exercise. Stroke volume, which can be varied over a smaller range by changing contractility, preload, or afterload. The demand for cardiac output varies with total tissue metabolism and is achieved through alterations in resistance to blood flow.

 

Because people differ in tissue mass, the need to compare cardiac outputs between individual requires an estimate of cardiac function that is normalized for body size. Such a measure is the Cardiac Index, defined as cardiac output divided by body surface area. Body surface area normalizes for different shapes, heights and weights. Tables are available that estimate body surface area from weight and height. An average surface area is 1.73 square meters (m2). Therefore a person with an average cardiac output of 5 l/min would have a Cardiac Index of:

 

5 l/min ÷ 1.73 m2 = 2.89 l/min/m2

 

The normal range for cardiac index is approximately 2.6-4.2. A cardiac index less than 2.5 may indicate mild left heart failure. Shock is suggested by a cardiac index less than 1.8.

 

Although the heart is driven by tissue demand, it can only pump the amount of blood that returns to it. Cardiac output is, therefore, limited by venous return. To make sense of this rather circular-seeming argument, a series of diagrams relating venous return and cardiac output have been developed.

 

  • Relationship of right atrial pressure and venous return.

The major determinant of venous return is the systemic filling pressure (PSF). This is the difference between peripheral venous pressure and right atrial pressure (Right atrial pressure is typically ~ 2 mmHg with a mean PSF of 7 mmHg. At this pressure difference (7 - 2) and the low resistance of the venous system, venous return is approximately 5 l/min (Fig. 1). Retention of salt and water, with its resulting increase of PSF, would increase the pressure difference and increase venous return (noted on the upper dotted line). On the other hand,

hemorrhage would reduce peripheral venous pressure and reduce venous return for a given right atrial pressure (noted in the lower dotted curve).

 

Further, if the ventricles failed to pump all the blood delivered to them, blood would accumulate in the atria thereby raising atrial pressure. The resulting increase in right atrial pressure would reduce the pressure difference between peripheral veins and the heart and reduce venous return. Fig. 1 captures the relationship between venous filling, atrial pressure, and venous return.

 

  • Relationship of right atrial pressure and cardiac output.

Right atrial pressure determines the extent of ventricular filling during diastole (preload). The relationship between preload, afterload and contractility can be understood by overlaying cardiac function curve (Fig. 2 and Fig. 3). These curves demonstrate the relationship between contractility and preload and cardiac output (venous return).

 

Reading from the normal contractility curve (Fig. 2), at a normal mean circulatory filling pressure of 7 mmHg, and a normal right atrial pressure of 2 mmHg, cardiac output is 5 l/min.

 

Assuming a constant systemic filling pressure an increase in cardiac contractility should increase stroke volume and cardiac output (Fig. 2). Two results of this change are noted on the upper curve above. First, cardiac output has increased with increased contractility. Secondly, more effective emptying of the ventricle should reduce right atrial pressure (systemic venous pressure).

It can be seen that reduced cardiac output and elevated right atrial pressure are the consequences of reduced cardiac contractility.

 

  • Venous return must equal cardiac output.

Over time cardiac output and venous return must be equal for each ventricle, although transient differences can occur. Changes in posture, such as lying down, can briefly increase venous return. The resulting change in the preload should increase cardiac output. But the vascular system is a closed circuit, blood pumped from the heart returns to the heart, therefore, venous return must equal cardiac output over time.

  • Cardiac Factors Determining Cardiac Output.

Since, Cardiac Output = Stroke Volume x Heart Rate, it is valuable to describe those factors that affect stroke volume and heart rate as determinants of cardiac output.

 

    • Summary of the determinants of stroke volume
      • Diastolic filling (EDV) is a determinant of stroke volume by determining ventricular preload.
      • Inotropic state (Contractility) can be affected by sympathetic nervous innervation and inotropic drugs such as the cardiac glycosides and sympathomimetic agonists.
      • Aortic pressure (and/or aortic valve diameter) is the major determinant of afterload on the left heart.
      • Effect of heart rate on stroke volume. Most ventricular filling occurs within the first third of diastole. Increasing heart rate reduces the duration of diastole and reduces the time for ventricular filling. However, increases of heart rate up to rates of 120 bpm have little effect on cardiac filling since they do not impinge on the early, rapid filling period. Limitations on filling may become apparent at heart rates, above 120 bpm if systemic filling pressure is not increased. However, during exercise with accompanying sympathetic stimulation cardiac output is proportional to heart rate up to 180 bpm. The stroke volume may be limited by further increases in heart rate. Cardiac output may actually fall because of decreased stroke volume, consequent to decreased filling time, at very high heart rates (>200 bpm).

 

    • Summary of Determinants of Heart Rate

The heart rate is primarily a function of the balance between sympathetic and parasympathetic input to the heart. At rest in humans, the parasympathetic influence dominates and the resting heart rate is slower than in a totally denervated heart.

 

Several minor factors also influence heart rate:

      • Chemical reactions proceed faster at elevated temperatures. Fever may cause an increase heart rate solely from the effect of temperature.
      • Metabolic activity of the pacemaker cells also affects heart rate. Increased metabolic activity (hyperthyroidism) may lead to increased heart rate.
      • As described previously, changes in extracellular ionic environment (hyperkalemia, hypokalemia, acidosis) may also alter heart rate.

 

  • Alterations in Cardiac Output in Health and Disease.

 

    • Exercise

Increased skeletal muscle metabolism increases the total O2 demands. Increased blood flow to muscle decreases peripheral resistance to flow. This, along with the muscle pumping action and respiratory pump action, increases venous return and cardiac output. Cardiac output can increase 4 to 6 fold in exercise.

 

In spite the reduced peripheral resistance, arterial pressure does not decrease in exercise because of the baroreceptor reflex.

 

    • Posture

Standing, after sitting or lying, decreases cardiac output by as much as 20% due to pooling of blood in the veins of the legs with a resultant reduction of venous return.

 

    • Pregnancy

Cardiac output increases by as much as 10% during pregnancy, partially due to the increased body mass and blood volume, but also due to the low resistance of the placental and uterine vasculature producing a shunt of blood from arterial to venous sides. Cardiac output is reflexly increased to maintain arterial pressure.

 

    • Anemia

Two factors increase cardiac output. Anemia lowers blood viscosity which marginally reduces resistance to blood flow. More importantly, anemia reduces O2 content of blood. Delivering more blood per minute to transport the same quantity of O2 must compensate this.

 

    • Hemorrhage

Decrease blood volume (decreased circulatory filling pressure) reduces venous return.

 

    • Metabolic

Hyperthyroidism, like fever and exercise, increases tissue metabolic activity and O2 demand.

 

    • Cardiac Failure

Includes syndromes in which myocardial cells fail to contract normally.

 

  • Measurement of Cardiac Output.

 

    • The Fick Method

Figure 4

Fick method of measuring cardiac output.

 

Flow can be measured by adding (or removing) a substance to the liquid as it passes through the tube. By knowing the quantity added per time and measuring the concentration of the substance in the effluent, the volume of liquid flowing through the tube per time can be calculated by the following formula:

Volume per time = Quantity added per time ÷ concentration in the effluent

 

To account for the possibility of the substance being present in the incoming fluid, the equation can be modified as follows:

 

Flow rate (volume/time) = Quantity added per time ÷ difference in concentration between the two ends of the tube

 

Relevant to the heart, blood is pumped from the venous system through the lungs to the arterial system. In the lungs, O2 is taken up into the blood stream. The O2 uptake can be measured at the mouth. Arterial and venous O2 concentrations can be measured by withdrawing and analyzing blood from both vessels. Therefore:

 

Cardiac Output = O2 consumption/min ÷ (aO2 - vO2)

 

This relatively simple procedure can be used to accurately estimate cardiac output. Variations on this procedure will be used to estimate renal blood flow later in the course.

(Reprinted from Circulatory Physiology-the essentials 2nd ed.,(1984) by J.J.smith & J.P. Kampine, Figure 7.6, page 122, Lippincott, Williams & Wilkins.)

    • Indicator-dilution method

A second technique is a variation on the Fick method. A known quantity of a dye is injected into the right atrium via catheter. Small amounts of blood are continuously withdrawn from the arterial system with an indwelling catheter and passed through a photosensitive device that measures dye concentration. The resulting curve measures dye concentration as a function of time.

The area under the dye-dilution curve can be calculated and approximates the average concentration of dye over time. Knowing the quantity of dye injected, the cardiac output can be determined by:

 

Cardiac output = Quantity of dye injected ÷ area under the curve

 

For both the Fick method and the Indicator-Dilution method, it is critical that the dye must be well mixed in the blood, should not be lost from the circulation, must not be toxic, or have any cardiac effects of its own.

 

Another variation on this theme is the Thermo-dilution technique in which a bolus of cold dextrose solution substitutes for the dye. The procedure is the same, but blood temperature is measured instead of dye color.

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