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Regulation of Stroke Volume

Venous Return

Frank-Starling mechanism (FSM): The heart autonomously responds to changes in ventricular volume load or aortic pressure load by adjusting the stroke volume (SV) in accordance with the myocardial preload (resting tension; ^ p. 66 ff.). The FSM also functions to maintain an equal SV in both ventricles to prevent congestion in the pulmonary or systemic circulation.

Preload change. When the volume load (preload) increases, the start of isovolumic contraction shifts to the right along the passive P-V curve (^ A1, from point A to point Ai). This increases end-diastolic volume (EDV), stroke volume (SV), cardiac work and end-systolic volume (ESV) (^ A).

Afterload change. When the aortic pressure load (afterload) increases, the aortic valve will not open until the pressure in the left ventricle has risen accordingly (^ A2, point Dt). Thus, the SVin the short transitional phase (SVt) will decrease, and ESV will rise (ESVt). Consequently, the start of the isovolumic contraction shifts to the right along the passive P-V curve (^ A2, point A2). SV will then normalize (SV2) despite the increased aortic pressure (D2), resulting in a relatively large increase in ESV (ESV2).

Preload or afterload-independent changes in myocardial contraction force are referred to as contractility or inotropism. It increases in response to norepinephrine (NE) and epinephrine (E) as well as to increases in heart rate (p1-adrenoceptor-mediated, positive inotropic effect and frequency inotropism, respectively; ^ p. 194). This causes a number of effects, particularly, an increase in isovolumic pressure peaks (^ A3, green curves). The heart can therefore pump against increased pressure levels (^ A3, point D3) and/or eject larger SVs (at the expense of the ESV) (^ A3, SV4).

While changes in the preload only affect the force of contraction (^ p. 203 B1), changes in contractility also affect the velocity of contraction (^ p. 203/B2). The steepest increase in isovolumic pressure per unit time (maximum dP/dt) is therefore used as a measure of contractility in clinical practice. dP/dt is increased E and NE and decreased by bradycardia (^ p. 203 B2) or heart failure.

Blood from the capillaries is collected in the veins and returned to the heart. The driving forces for this venous return (^ B) are: (a) vis a tergo, i.e., the postcapillary blood pressure (BP) (ca. 15 mmHg); (b) the suction that arises due to lowering of the cardiac valve plane in systole; (c) the pressure exerted on the veins during skeletal muscle contraction (muscle pump); the valves of veins prevent the blood from flowing in the wrong direction, (d) the increased abdominal pressure together with the lowered intrathoracic pressure during inspiration (Ppl; ^ p. 108), which leads to thoracic venous dilatation and suction (^ p. 206).

Orthostatic reflex. When rising from a supine to a standing position (orthostatic change), the blood vessels in the legs are subjected to additional hydrostatic pressure from the blood column. The resulting vasodilation raises blood volume in the leg veins (by ca. 0.4 L). Since this blood is taken from the central blood volume, i.e., mainly from pulmonary vessels, venous return to the left atrium decreases, resulting in a decrease in stroke volume and cardiac output. A reflexive increase (orthostatic reflex) in heart rate and peripheral resistance therefore occurs to prevent an excessive drop in arterial BP (^ pp. 7 E and 212 ff.); orthostatic collapse can occur. The drop in central blood volume is more pronounced when standing than when walking due to muscle pump activity. Conversely, pressure in veins above the heart level, e.g., in the cerebral veins, decreases when a person stands still for prolonged periods of time. Since the venous pressure just below the diaphragm remains constant despite changes in body position, it is referred to as a hydrostatic indifference point.

The central venous pressure (CVP) is measured at the right atrium (normal range: 0-12 cm H2O or 0-9 mmHg). Since it is mainly dependent on the blood volume, the CVP is used to monitor the blood volume in clinical medicine (e.g., during a transfusion). Elevated CVP (> 20 cm H2O or 15 mmHg) may be pathological (e.g., due to heart failure or other diseases associated with cardiac pump dysfunction), or physiological (e.g., in pregnancy).

|ā€” A. Factors influencing cardiac action

1 Increase in filling (preload)

2 Increase in blood pressure (afterload)

1 Increase in filling (preload)

2 Increase in blood pressure (afterload)

EDV f

3 Increase in contractility

3 Increase in contractility

B. Venous return

Venous return = cardiac output

Right heart

Left heart

Suction via lowering of cardiac valve plane

Venous return = cardiac output

Right heart

Left heart

Suction via lowering of cardiac valve plane

Systemic

Blood pressure H. circulation ca. 15mmHg

Arterial Blood Pressure

The term blood pressure (BP) per se refers to the arterial BP in the systemic circulation. The maximum BP occurs in the aorta during the systolic ejection phase; this is the systolic pressure (Ps); the minimum aortic pressure is reached during the isovolumic contraction phase (while the aortic valves are closed) and is referred to as the diastolic pressure (Pd) (^ A1 and p. 191, phase I in A2). The systolic-diastolic pressure difference (Ps-Pd) represents the blood pressure amplitude, also called pulse pressure (PP), and is a function of the stroke volume (SV) and arterial compliance (C = dV/dP, ^ p. 188). When C decreases at a constant SV, the systolic pressure Ps will rise more sharply than the diastolic pressure Pd, i.e., the PP will increase (common in the elderly; described below). The same holds true when the SV increases at a constant C.

If the total peripheral resistance (TPR, ^ p. 188) increases while the SV ejection time remains constant, then Ps and the Pd will increase by the same amount (no change in PP). However, increases in the TPR normally lead to retardation of SV ejection and a decrease in the ratio of arterial volume rise to peripheral drainage during the ejection phase. Consequently, Ps rises less sharply than Pd and PP decreases.

Normal range. In individuals up to 45 years of age, Pd normally range from 60 to 90mmHg and Ps from 100 to 140 mmHg at rest (while sitting or reclining). A Ps of up to 150 mmHg is considered to be normal in 45 to 60-year-old adults, and a Ps of up to 160 mmHg is normal in individuals over 60 (^ C). Optimal BP regulation (^ p. 212) is essential for proper tissue perfusion.

Abnormally low BP (hypotension) can lead to shock (^ p. 218), anoxia (^ p. 130) and tissue destruction. Chronically elevated BP (hypertension; ^ p. 216) also causes damage because important vessels (especially those of the heart, brain, kidneys and retina) are injured.

The mean BP (=the average measured over time) is the decisive factor ofperipheral perfusion (^ p. 188).

The mean BP can be determined by continuous BP measurement using an arterial catheter, etc. (^ A).

By attenuating the pressure signal, only the mean BP is recorded.

Although the mean BP falls slightly as the blood travels from the aorta to the arteries, the Ps in the greater arteries (e.g., femoral artery) is usually higher than in the aorta (A1 v. A2 ) because their compliance is lower than that of the aorta (see pulse wave velocity, p. 190).

Direct invasive BP measurements show that the BP curve in arteries distal to the heart is not synchronous with that of the aorta due to the time delay required for passage of the pulse wave (3-10 m/s; ^ p. 190); its shape is also different (^ A1/A2).

The BP is routinely measured externally (at the level of the heart) according to the Riva-Rocci method by sphygmomanometer (^ B). An inflatable cuff is snuglywrapped around the arm and a stethoscope is placed over the brachial artery at the crook of the elbow. While reading the manometer, the cuff is inflated to a pressure higher than the expected Ps (the radial pulse disappears). The air in the cuff is then slowly released (2-4mmHg/s). The first sounds synchronous with the pulse (Korotkoff sounds) indicate that the cuff pressure has fallen below the Ps. This value is read from the manometer. These sounds first become increasingly louder, then more quiet and muffled and eventually disappear when the cuff pressure falls below the Pd (second reading).

Reasons for false BP readings. When re-measuring the blood pressure, the cuff pressure must be completely released for 1 to 2 min. Otherwise venous pooling can mimic elevated Pd. The cuff of the sphygmomanometer should be 20% broader than the diameter of the patient's upper arm. Falsely high Pd readings can also occur if the cuff is too loose or too small relative to the arm diameter (e.g., in obese or very muscular patients) or if measurement has to be made at the thigh.

The blood pressure in the pulmonary artery is much lower than the aortic pressure (^ p. 186). The pulmonary vessels have relatively thin walls and their environment (air-filled lung tissue) is highly compliant. Increased cardiac output from the right ventricle therefore leads to expansion and thus to decreased resistance of the pulmonary vessels (^ D). This prevents excessive rises in pulmonary artery pressure during physical exertion when cardiac output rises. The pulmonary vessels also function to buffer short-term fluctuations in blood volume (^ p. 204).

iā€” A. Arterial blood-pressure curve

Pulse pressure (PS-PD)

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