книги студ / color atlas of physiology 5th ed[1]. (a. despopoulos et al, thieme 2003)

(#+ 120") can develop due right ventricular hypertrophy, while left axis deviation (more negative than –30") can occur due to left ventricular hypertrophy.

An extensive myocardial infarction (MI) can shift the electrical axis of the heart. Marked Q wave abnormality (!I 1) is typical in transmural myocardial infarction (involving entire thickness of ventricular wall): Q wave duration #0.04 s and Q wave amplitude #25% of total amplitude of the QRS complex. These changes appear within 24 hours of MI and are caused by failure of the dead myocardium to conduct electrical impulses. Preponderance of the exci-

198tatory vector in the healthy contralateral side of the heart therefore occurs while the affected part of the

myocardium should be depolarizing (first 0.04 s of QRS). The so-called “0.04-sec vector” is therefore said to point away from the infarction. Anterior MI is detected as highly negative Q waves (with smaller R waves) mainly in leads V5, V6, I and aVL. Q wave abnormalities can persist for years after MI (!I 2/3), so they may not necessarily be indicative of an acute infarction. ST elevation points to ischemic but not (yet) necrotic parts of the myocardium. This can be observed: (1) in myocardial ischemia (angina pectoris),

(2) in the initial phase of transmural MI, (3) in nontransmural MI, and (4) along the margins of a transmural MI that occurred a few hours to a few days prior (!I 4). The ST segment normalizes within 1 to 2 days of MI, but the T wave remains inverted for a couple of weeks (!I 5 and 2).

Excitation in Electrolyte Disturbances

Hyperkalemia. Mild hyperkalemia causes various changes, like elevation of the MDP (!p. 192) in the SA node. It can sometimes have positive chronotropic effects (!p. 193 B3c). In severe hyperkalemia, the more positive MDP leads to the inactivation of Na+ channels (!p. 46) and to a reduction in the slope and amplitude of APs in the AV node (negative dromotropic effect; !p. 193 B4). Moreover, the K+ conductance (gK) rises, and the PP slope becomes flatter due to a negative chronotropic effect (!p. 193 B3a). Faster myocardial repolarization decreases the cytosolic Ca2+ conc. In extreme cases, the pacemaker is also brought to a standstill (cardiac paralysis). Hypokalemia (moderate) has positive chronotropic and inotropic effects (!p. 193 B3a), whereas hypercalcemia is thought to raise the gK and thereby shortens the duration of the myocardial AP.

ECG. Changes in serum K+ and Ca2+ induce characteristic changes in myocardial excitation.

Hyperkalemia (#6.5 mmol/L): tall, peaked T waves and conduction disturbances associated with an increased PQ interval and a widened QRS. Cardiac arrest can occur in extreme cases.

Hypokalemia (!2.5 mmol/L): ST depression, biphasic T wave (first positive, then negative) followed by a positive U wave.

Hypercalcemia (#2.75 mmol/L total calcium): shortened QT interval due to a shortened ST segment.

Hypocalcemia (!2.25 mmol/L total calcium): prolonged QT interval.

8 Cardiovascular System

200

Ventricular Pressure–Volume

Relationships

phase, the pressure in the left ventricle rises (all valves closed) until the diastolic aortic pressure (80 mmHg in this case) is reached (!A1, point D). The aortic valve then opens. During the ejection phase, the ventricular volume is reduced by the stroke volume (SV) while the pressure initially continues to rise (!p. 188, Laplace’s law, Eq. 8.4b: Ptm " because r #and w "). Once maximum (systolic) pressure is reached (!A1, point S), the volume will remain virtually constant, but the pressure will drop slightly until it falls below the aortic pressure, causing the aortic valve to close (!A1, point K). During the isovolumetric relaxation phase, the pressure rapidly decreases to (almost) 0 (!A1, point V). The ventricles now contain only the end-systolic volume (ESV), which equals 60 mL in the illustrated example. The ventricular pressure rises slightly during the filling phase (passive pressure–volume curve).

Cardiac Work and Cardiac Power

Since work (J = N · m) equals pressure (N · m–2= Pa) times volume (m3), the area within the working diagram (!A1, pink area) represents the pressure/volume (P/V) work achieved by the left ventricle during systole (13,333 Pa· 0.00008 m3 = 1.07 J; right ventricle: 0.16 J). In systole, the bulk of cardiac work is achieved by active contraction of the myocardium, while a much smaller portion is attributable to passive elastic recoil of the ventricle, which stretches while filling. This represents diastolic filling work (!A1, blue area under the blue curve), which is shared by the ventricular myocardium (indirectly), the atrial myocardium, and the respiratory and skeletal muscles (!p. 204, venous return).

Total cardiac work. In addition to the cardiac work performed by the left and right ventricles in systole (ca. 1.2 J at rest), the heart has to generate 20% more energy (0.24 J) for the pulse wave (!p. 188, windkessel). Only a small amount of energy is required to accelerate the blood at rest (1% of total cardiac work), but the energy requirement rises with the heart rate. The total cardiac power (= work/time, !p. 374) at rest (70 min–1 = 1.17 s–1) is approximately 1.45 J · 1.17 s–1 = 1.7 W.

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 212ff.); 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).

A. Factors influencing cardiac action

1 Increase in filling (preload)

V4

Ventricular volume

SV

SV4

2 Increase in blood pressure (afterload)

Ventricular volume

B. Venous return

Venous return = cardiac output

Suction via lowering of cardiac valve plane

Negative pressure in thorax

Positive pressure in abdominal cavity

Muscle pump

Systemic

Blood pressure circulation ca. 15mmHg

Plate 8.10 Regulation of Stroke Volume

205

Arterial Blood Pressure

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 snugly wrapped 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 (2–4 mmHg/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-measur- ing 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 (airfilled 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).