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Ganong's Review of Medical Physiology, 23rd Edition

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578 SECTION VI Cardiovascular <strong>Physiology</strong><br />

CLINICAL BOX 34–3<br />

Stroke<br />

When the blood supply to a part <strong>of</strong> the brain is interrupted,<br />

ischemia damages or kills the cells in the area, producing<br />

the signs and symptoms <strong>of</strong> a stroke. There are two general<br />

types <strong>of</strong> strokes: hemorrhagic and ischemic. Hemorrhagic<br />

stroke occurs when a cerebral artery or arteriole ruptures,<br />

sometimes but not always at the site <strong>of</strong> a small aneurysm.<br />

Ischemic stroke occurs when flow in a vessel is compromised<br />

by atherosclerotic plaques on which thrombi form.<br />

Thrombi may also be produced elsewhere (eg, in the atria<br />

in patients with atrial fibrillation) and pass to the brain as<br />

emboli where they then lodge and interrupt flow. In the<br />

past, little could be done to modify the course <strong>of</strong> a stroke<br />

and its consequences. However, it has now become clear<br />

that in the penumbra, the area surrounding the most severe<br />

brain damage, ischemia reduces glutamate uptake by<br />

astrocytes, and the increase in local glutamate causes excitotoxic<br />

damage and death to neurons (see Chapter 7). In<br />

experimental animals, and perhaps in humans, drugs that<br />

prevent this excitotoxic damage significantly reduce the effects<br />

<strong>of</strong> strokes. In addition, clot-lysing drugs such as tissuetype<br />

plasminogen activator (t-PA) (see Chapter 32) are <strong>of</strong><br />

benefit in ischemic strokes. Both antiexcitotoxic treatment<br />

and t-PA must be given early in the course <strong>of</strong> a stroke to be<br />

<strong>of</strong> maximum benefit, and this is why stroke has become a<br />

condition in which rapid diagnosis and treatment have become<br />

important. In addition, <strong>of</strong> course, it is important to<br />

determine if a stroke is thrombotic or hemorrhagic, since<br />

clot lysis is contraindicated in the latter.<br />

cardiac veins (Figure 34–12), which drain into the right atrium.<br />

In addition, there are other vessels that empty directly<br />

into the heart chambers. These include arteriosinusoidal vessels,<br />

sinusoidal capillary-like vessels that connect arterioles to<br />

the chambers; thebesian veins that connect capillaries to the<br />

chambers; and a few arterioluminal vessels that are small arteries<br />

draining directly into the chambers. A few anastomoses<br />

occur between the coronary arterioles and extracardiac arterioles,<br />

especially around the mouths <strong>of</strong> the great veins. Anastomoses<br />

between coronary arterioles in humans only pass<br />

particles less than 40 μm in diameter, but evidence indicates<br />

that these channels enlarge and increase in number in patients<br />

with coronary artery disease.<br />

PRESSURE GRADIENTS & FLOW<br />

IN THE CORONARY VESSELS<br />

The heart is a muscle that, like skeletal muscle, compresses its<br />

blood vessels when it contracts. The pressure inside the left<br />

ventricle is slightly higher than in the aorta during systole<br />

Marginal<br />

branch<br />

Right coronary<br />

artery<br />

Left coronary<br />

artery<br />

Circumflex branch<br />

Anterior<br />

descending<br />

branch<br />

Septal<br />

branches<br />

Marginal<br />

branch<br />

FIGURE 34–11 Coronary arteries and their principal<br />

branches in humans. (Reproduced with permission from Ross G: The<br />

cardiovascular system. In: Essentials <strong>of</strong> Human <strong>Physiology</strong>. Ross G [editor]. Copyright ©<br />

1978 by Year Book <strong>Medical</strong> Publishers.)<br />

(Table 34–4). Consequently, flow occurs in the arteries supplying<br />

the subendocardial portion <strong>of</strong> the left ventricle only<br />

during diastole, although the force is sufficiently dissipated in<br />

the more superficial portions <strong>of</strong> the left ventricular myocardium<br />

to permit some flow in this region throughout the cardiac<br />

cycle. Because diastole is shorter when the heart rate is high,<br />

left ventricular coronary flow is reduced during tachycardia.<br />

On the other hand, the pressure differential between the aorta<br />

and the right ventricle, and the differential between the aorta<br />

and the atria, are somewhat greater during systole than during<br />

diastole. Consequently, coronary flow in those parts <strong>of</strong> the<br />

heart is not appreciably reduced during systole. Flow in the<br />

right and left coronary arteries is shown in Figure 34–13. Because<br />

no blood flow occurs during systole in the subendocardial<br />

portion <strong>of</strong> the left ventricle, this region is prone to<br />

ischemic damage and is the most common site <strong>of</strong> myocardial<br />

infarction. Blood flow to the left ventricle is decreased in<br />

Extracoronary<br />

arteries<br />

Arterioles<br />

Posterior descending branch<br />

Arteriosinusoidal<br />

vessels<br />

Coronary<br />

arteries<br />

Arterioles<br />

Capillaries<br />

Veins<br />

Coronary sinus or<br />

anterior cardiac<br />

veins<br />

Heart chambers<br />

Arterioluminal<br />

vessels<br />

Thebesian<br />

veins<br />

FIGURE 34–12 Diagram <strong>of</strong> the coronary circulation.

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