Body Fluids and Circulation: Class 11 Biology · Chapter 15

Roughly 30 trillion cells make up your body, and hardly any of them touch the outside world. A cell deep in your liver cannot reach for air or water. Oxygen, glucose and amino acids have to be brought to it, and its carbon dioxide and urea have to be taken away before they build up. Diffusion alone handles this only over very short distances: it carries oxygen across a few cells in a fraction of a second, but needs hours to cover a centimetre. Any animal more than a few millimetres thick therefore needs a transport system.

Evolution has produced two broad answers. One is to let the surroundings do the carrying: sponges and coelenterates such as Hydra keep outside water flowing through canals and cavities in the body, and each cell swaps materials with that passing stream. The other, used by larger animals, is an internal fluid driven past every cell. For us that fluid is blood, backed up by a second fluid, lymph. This chapter takes both fluids apart, then follows the heart and vessels that keep blood moving, the controls that adjust them and the disorders that upset them.

15.1 Blood

Put a drop of blood under a microscope and the even red colour disappears. You see cells and cell fragments drifting in a pale liquid, like grains of sabudana in water. Biologists class blood as a connective tissue, though an unusual one. Its cells are not packed together but suspended in a liquid matrix, the plasma, and the suspended parts are called the formed elements. Like other connective tissues it develops from mesoderm, and it links every organ with every other by carrying materials between them.

15.1.1 Plasma

Plasma (प्लाज़्मा) is a thick, slightly viscous liquid, pale yellow like straw, that forms a little over half of blood, about 55 per cent. Water makes up 90–92 per cent of it, which is why it dissolves and carries so much. Proteins account for another 6–8 per cent, and three of them dominate (Table 15.1).

The last one or two per cent is a mixed cargo. Mineral ions such as $\mathrm{N}\mathrm{a}{\phantom{X}}^{+}$, $\mathrm{C}\mathrm{a}{\phantom{X}}^{2+}$, $\mathrm{M}\mathrm{g}{\phantom{X}}^{2+}$, $\mathrm{H}\mathrm{C}\mathrm{O}{\phantom{X}}_3{\phantom{X}}^{-}$ and $\mathrm{C}\mathrm{l}{\phantom{X}}^{-}$ keep the salt balance and pH steady. Plasma is also the body's delivery van: glucose, amino acids and lipids absorbed from the gut or released from stores ride in it to the tissues that use them, so some of each is there at any moment. Plasma also carries a set of clotting factors, kept switched off until an injury activates them. Take these factors away, as happens when blood clots in a tube, and the clear fluid left is serum.

15.1.2 Formed Elements

The formed elements (संगठित पदार्थ) make up the remaining 45 per cent or so of blood. They are of three kinds: red blood cells or erythrocytes, white blood cells or leucocytes, and platelets, also called thrombocytes. Fig. 15.2 lines them up side by side.

The job of an erythrocyte is to carry respiratory gases, and its whole design serves that job. It is packed with haemoglobin (हीमोग्लोबिन), a red, iron-containing protein that gives the cells, and blood, their colour; a healthy person's blood holds 12–16 g of it per 100 mL. To make room, the RBC of most mammals throws out its nucleus as it matures, and it settles into a disc pinched in on both faces, a biconcave shape. In adults these cells are made in the red bone marrow, and they outnumber every other cell in blood: a healthy adult man has about 5 to 5.5 million in each cubic millimetre.

Having no nucleus has a cost: an RBC cannot make new proteins to repair itself. After about 120 days of squeezing through narrow capillaries it wears out and is broken down, mainly in the spleen, which has earned the nickname 'graveyard of RBCs'. To hold the count steady, the bone marrow must replace old cells as fast as they are lost, and Example 15.1 shows just how fast that is.

White blood cells, or leucocytes, are far fewer: 6000–8000 per cubic millimetre on average, roughly one for every 700 red cells. Each has a nucleus but no haemoglobin, which is why they look colourless, and most live only a short time. Stained under a microscope they fall into two groups: granulocytes (neutrophils, eosinophils and basophils), whose cytoplasm is packed with visible granules, and agranulocytes (lymphocytes and monocytes), which lack obvious granules. Table 15.2 compares the five.

Think of the five as a defence force with different duties. Lymphocytes, in two main forms, B and T lymphocytes, run the body's immune responses, which you will study in Class 12. Neutrophils and monocytes are the clean-up crew: they are phagocytes that engulf and destroy bacteria and other foreign organisms that get in. Eosinophils help resist infections, notably by parasitic worms, and are involved in allergic reactions. Basophils release histamine, serotonin and heparin, chemicals that drive inflammation, the redness and swelling around an infected cut.

Platelets are not whole cells but tiny fragments budded off megakaryocytes, giant cells in the bone marrow. A cubic millimetre of blood normally holds 1.5–3.5 lakh (150 000–350 000) of them. Their main duty is to start clotting: at a damaged vessel they gather and pour out chemicals that switch on the clotting process (Section 15.1.4). So when the count falls, as it can in dengue, a person bruises easily and bleeding is hard to stop.

15.1.3 Blood Groups

Two samples of healthy blood look identical in a test tube, yet mixing them can be dangerous. The difference lies in molecules on the surface of the red cells. An antigen (प्रतिजन) is a chemical that can set off an immune response; an antibody is a protein made by the body that binds a particular antigen. When antibodies meet red cells carrying their matching antigen, they bind several cells together into clumps (agglutination), and the clumped cells are destroyed. More than forty blood-group systems are known, but transfusion services everywhere check two of them first: ABO and Rh.

15.1.3.1 ABO grouping

The ABO system depends on two antigens, A and B, which may or may not be present on a person's red cells. Cells with A only give group A, with B only group B, with both group AB, and with neither group O. The plasma carries natural antibodies against whichever of the two antigens the person's own cells lack. Group A plasma therefore has anti-B, group B plasma has anti-A, group O plasma has both and group AB plasma has neither (Table 15.3, Fig. 15.3).

The rule behind the last two columns of the table is a single question: will the recipient's antibodies find a matching antigen on the donor's red cells? Group O cells carry neither A nor B, so no recipient's antibodies can latch on to them, and group O people are called universal donors. Group AB plasma contains neither antibody, so people of group AB can accept cells of any ABO group and are called universal recipients. 11The donor's own antibodies are usually ignored because they are diluted in the recipient's much larger blood volume. In practice hospitals give red cells of the matching group whenever they can.

15.1.3.2 Rh grouping

Red cells may carry one more antigen that matters for transfusion. It is called the Rh antigen (Rh factor) because a similar molecule was found on the red cells of rhesus monkeys. If your red cells have it you are Rh positive (Rh+); if not, Rh negative (Rh−). NCERT puts the Rh+ share at nearly 80 per cent of humans; it varies between populations, and in India only about 5–7 per cent of blood donors test Rh−.

Anti-Rh antibodies behave differently from anti-A and anti-B: they are not present from birth. An Rh− person starts making them only after Rh+ red cells enter the body, for instance through a mismatched transfusion. That first exposure sensitises the person, and a second one can then trigger a severe reaction. So Rh type is matched along with ABO group before every transfusion.

Pregnancy can cause the same exposure without any transfusion, when an Rh− mother carries an Rh+ baby (the father is Rh+). Follow the story in Fig. 15.4 through three questions.

• Why is the first such baby usually safe? Until birth the placenta keeps the two bloodstreams apart, so the mother's immune system never meets the foetus's Rh antigen and no anti-Rh antibodies exist yet. At delivery, though, a little of the baby's blood can leak into her circulation, and her body begins to make anti-Rh antibodies.
• Why is a later Rh+ baby at risk? Unlike red cells, these antibodies can pass across the placenta. In her next Rh+ pregnancy they enter the foetus and destroy its red cells, causing severe anaemia and jaundice, sometimes death. This is erythroblastosis foetalis (गर्भ रक्ताणु कोरकता), named after the immature red cells (erythroblasts) that flood the baby's blood as its marrow struggles to keep up.
• How is it prevented? Straight after the first delivery (in practice within about 72 hours) the mother is injected with anti-Rh antibodies. They clear the baby's Rh+ cells from her blood before her own immune system responds, so she is never sensitised and the next baby is protected.

15.1.4 Coagulation of Blood

A paper cut bleeds for a minute or two and then stops, even though the tiny vessels in it are still torn. Something has plugged the leaks. That plug is a clot (coagulum), and the process that forms it, coagulation (रुधिर स्कंदन), protects the body from losing too much blood whenever it is injured.

Under a microscope a clot turns out to be a tangle of fine protein threads, fibrin, in which red cells, platelets and other formed elements, many of them damaged, are caught like fish in a net. Fibrin does not float around ready-made. It is produced on the spot from the soluble plasma protein fibrinogen, at the end of a chain of reactions in which each activated substance switches on the next. Such a chain is called a cascade (Fig. 15.6).

1. Damaged tissue and the platelets gathering at a wound release factors that start the cascade. Either source alone can set it off.
2. Clotting factors carried inactive in the plasma then activate one another in turn, producing an enzyme complex, thrombokinase.
3. Thrombokinase converts the inactive plasma protein prothrombin into the active enzyme thrombin.
4. Thrombin converts soluble fibrinogen into insoluble fibrin threads, and their mesh traps blood cells to form the clot.

Calcium ions ($\mathrm{C}\mathrm{a}{\phantom{X}}^{2+}$) are needed at several steps, so blood short of free calcium cannot clot. Why use a long cascade instead of one reaction? Each activated enzyme molecule activates many molecules of the next substance, so a small trigger at a wound is quickly amplified into enough fibrin to seal it, while blood elsewhere stays liquid.

15.2 Lymph (Tissue Fluid)

A capillary behaves like the soaker hoses used to water kitchen gardens. Its wall is a single layer of cells, and the pressure of the blood inside forces liquid out through it. What seeps out is a filtrate of plasma: water, ions, glucose and other small molecules pass easily, while plasma proteins and blood cells are too large and stay behind. This filtrate, bathing the cells of every tissue, is tissue fluid (interstitial fluid): it carries the same mineral ions as plasma but far less protein.

No cell touches blood directly; oxygen, nutrients and wastes always cross this fluid on their way in or out. If all the filtrate stayed put, tissues would swell, so it has to be drained. Most of it soaks back into the capillaries. The rest is picked up by blind-ended lymph capillaries and carried along a branching network of vessels, the lymphatic system, which empties into large veins at the base of the neck. Inside these vessels the same fluid is called lymph (लसीका) (Fig. 15.7).

Lymph has no red cells, so it is colourless. Its main cells are lymphocytes, which multiply in the lymph nodes strung along the vessels, so the lymphatic system is also a key part of the body's immune defences. Lymph is a transport route too: hormones and nutrients travel in it, and digested fats leave the gut this way. Each villus of the small intestine holds a lymph vessel, the lacteal, that absorbs fat, which reaches the blood only after a trip through the lymph.

15.3 Circulatory Pathways

Animals pump blood in one of two ways, and the difference is what happens after the blood leaves the heart (Fig. 15.8). In insects, prawns, spiders, snails and mussels (arthropods and molluscs), the heart drives blood through a few large vessels that simply end. The blood pours out into open spaces among the organs, the sinuses, bathes the tissues directly and drifts back to the heart: an open circulatory system. 22Cephalopod molluscs such as the octopus and squid are an exception: their circulation is largely closed. Earthworms and other annelids, and all chordates including us, keep their blood inside an unbroken loop of vessels, and materials reach the cells only across thin capillary walls: a closed circulatory system.

Keeping blood inside vessels has a big payoff: the body can steer it. By widening some vessels and narrowing others, it sends more blood to the leg muscles during a run, to the gut after lunch or to the skin on a hot afternoon. Pressure can also be kept higher, so blood moves faster. This is why a closed system is considered the more advantageous of the two.

Every vertebrate has a closed system driven by a muscular heart with chambers. What changed during vertebrate evolution is the number of chambers, and with it how well blood rich in oxygen is kept apart from blood that has given up its oxygen (Fig. 15.9, Table 15.4).

• Fishes have a two-chambered heart, one atrium and one ventricle. It receives only deoxygenated blood from the body and pumps it to the gills; there the blood takes up oxygen and flows straight on to the body before returning to the heart. Blood passes through the heart once per round trip: single circulation.
• Amphibians and most reptiles have three chambers: two atria and a single ventricle. Oxygenated blood returning from the lungs, skin or gills enters the left atrium, while deoxygenated blood from the body enters the right atrium. Both atria empty into the one ventricle, where the two streams partly mix, so what leaves the ventricle is a blend of both. Blood does return to the heart twice, but the two circuits are not separated: incomplete double circulation.
• Crocodiles, birds and mammals have four chambers: two atria and two ventricles. The right side of the heart handles only oxygen-poor blood and the left side only oxygen-rich blood, with a complete wall between them, so the two streams stay separate. These animals have two separate circuits and so a full double circulation (Section 15.4).

15.3.1 Human Circulatory System

Three things make up our blood vascular system: the blood itself, the vessels that carry it (a closed, branching network) and the muscular, chambered heart that drives it.

Make a fist: that is roughly the size of your heart. It sits in the thoracic cavity between the two lungs, tilted slightly to the left, inside a two-layered bag, the pericardium; the pericardial fluid between the layers lets it beat without friction. Like blood and muscle, the heart develops from mesoderm.

The heart is a double pump with four chambers (Fig. 15.10): two smaller upper atria (singular atrium) that receive blood and two larger lower ventricles that pump it out. Three walls, or septa, divide them, as Table 15.5 shows; the septum between each atrium and the ventricle below it has an opening that connects the two chambers of that side.

Four valves make the flow one-way. Each is pushed open when blood moves forward and slams shut when blood tries to go back:

• right atrium → right ventricle: the tricuspid valve, with three flaps (cusps);
• left atrium → left ventricle: the bicuspid or mitral valve, with two;
• right ventricle → pulmonary artery and left ventricle → aorta: the semilunar valves, named after their half-moon-shaped cusps.

Tough cords, the chordae tendineae, tie the cusps of the tricuspid and bicuspid valves to the ventricle walls so that they cannot flip back into the atria. Blood can therefore travel only one way: atrium to ventricle, then ventricle to artery, never back.

The whole heart is built of cardiac muscle. The ventricle walls are much thicker than the atrial walls: the atria only have to top up the ventricles just below them, while the ventricles must drive blood out of the heart, and the left ventricle, which supplies the whole body, has the thickest wall of all.

Running through this muscle is a specialised kind of cardiac muscle, the nodal tissue, which generates and conducts the electrical signals that make the heart beat (Fig. 15.11). Its parts form a pathway:

1. the sino-atrial node (SAN, शिरा-अलिंद पर्व), a patch in the upper right corner of the right atrium;
2. the atrio-ventricular node (AVN), at the bottom of the right atrium on its left side, just above the atrioventricular septum;
3. the atrio-ventricular bundle (AV bundle, or bundle of His), a bundle of nodal fibres that runs from the AVN through the atrioventricular septum to the top of the interventricular septum, where it splits into a right and a left bundle branch;
4. the Purkinje fibres, fine branches that spread from each bundle branch through the muscle of its ventricle.

Why does the heart need no order from the brain to beat? Nodal tissue is autoexcitable: its cells fire action potentials spontaneously, with no outside stimulus. Different parts fire at different natural rates, and the SAN is the quickest, at about 70–75 a minute. Like the fastest drummer in a band, it sets the tempo: each SAN impulse sweeps through the heart and triggers a beat before the slower parts reach their own firing point. The SAN is therefore the heart's pacemaker, and a normal resting heart rate, 70–75 beats a minute (72 on average), is simply its firing rate. The AVN delays the signal slightly, which gives the atria time to finish emptying before the ventricles contract.

15.3.2 Cardiac Cycle

Each heartbeat is the same sequence of squeezing and relaxing, repeated about 72 times a minute. Contraction of a chamber is called systole and relaxation diastole. One rule explains every valve movement in the sequence: a valve has no muscle of its own, so it simply opens when the pressure behind it is higher than the pressure in front, and shuts when blood tries to flow the other way. With that rule in mind, follow one round in Fig. 15.12, starting from a moment when all four chambers are relaxed.

1. Joint diastole. With every chamber relaxed, the tricuspid and bicuspid valves hang open and the semilunar valves are shut. Blood arriving through the venae cavae and the pulmonary veins passes through the atria and into the ventricles, which fill passively.
2. Atrial systole. An action potential from the SAN makes both atria contract together. They squeeze in the last of the filling blood, boosting ventricular filling by roughly 30 per cent.
3. Ventricular systole. The signal crosses to the ventricles through the AVN and the AV bundle, and the bundle of His and its fibres spread it through the ventricular muscle. The ventricles contract while the atria relax. As ventricular pressure climbs, blood is pushed back towards the atria and the tricuspid and bicuspid valves are forced shut.
4. Ejection. Pressure keeps rising until it is higher than the pressure in the pulmonary artery and the aorta. The semilunar valves are pushed open and blood leaves the heart.
5. Ventricular diastole. The ventricles relax and their pressure falls below that in the arteries. Blood starting to slip back closes the semilunar valves.
6. Refilling. Ventricular pressure keeps falling until it is below the pressure in the atria, which have been filling from the veins all along. Atrial pressure now wins, the tricuspid and bicuspid valves swing open, blood flows into the ventricles again, and the heart is back in joint diastole until the SAN fires again.

One complete round of these events, from one atrial systole to the next, makes up a cardiac cycle (हृद् चक्र): in it the atria and the ventricles each contract (systole) and relax (diastole) once. One heartbeat is one cycle, so its duration follows from the heart rate:

At 72 beats a minute, $60\mathrm{/}72\approx 0.83$, so each cycle lasts about 0.8 s. 33At 72 beats a minute the atria are in systole for roughly 0.1 s and the ventricles for roughly 0.3 s; for about 0.4 s all four chambers rest together. These approximate timings are extra detail, not part of the NCERT text. In each cycle a ventricle pumps out about 70 mL of blood; this is its stroke volume. The volume of blood each ventricle pumps in one minute is the cardiac output (हृद् निकास).

For a resting adult, 70 mL × 72 per minute ≈ 5000 mL, about 5 L of blood a minute from each ventricle. The body adjusts both factors to match demand. During exercise nerves and hormones raise the heart rate and strengthen each contraction, so cardiac output can rise to several times its resting value. Regular training enlarges and strengthens the heart, so an athlete's stroke volume is bigger, the resting heart rate is often lower, and the maximum cardiac output is much higher than an untrained person's (Example 15.2).

The familiar 'lub–dub' of a heartbeat is not the sound of muscle squeezing; it is the sound of valves snapping shut. The first, longer and duller lub is made when the tricuspid and bicuspid valves close as ventricular systole begins. The second, shorter and sharper dub is made when the semilunar valves close as the ventricles relax. A valve that does not close properly lets blood leak back with an extra whooshing sound, a murmur, which is why doctors listen to these sounds through a stethoscope to diagnose heart problems.

15.3.3 Electrocardiogram (ECG)

Every contraction you followed in Section 15.3.2 begins as an electrical signal. A tiny part of that electricity spreads through the body to the skin, where electrodes can detect it. The machine that records it is an electrocardiograph, and its record is an electrocardiogram or ECG (विद्युत हृद्लेख): a graph of the heart's electrical activity through each cardiac cycle.

Three electrodes are enough for a standard ECG: one clipped to each wrist and one to the left ankle, and the machine records for as long as they stay on. A cardiologist who wants more detail adds a row of extra electrodes across the chest; this chapter sticks to the three-lead version. The peaks and dips of the trace are named with the letters P to T (Fig. 15.14):

• P wave: a wave of depolarisation (electrical excitation) spreads over both atria, and their contraction follows.
• QRS complex: the ventricles depolarise. They begin to contract a moment after Q, so the QRS complex signals the onset of ventricular systole.
• T wave: the ventricles repolarise, recovering from excitation to their resting state. When the T wave finishes, systole is over.

Each QRS complex is one ventricular beat, so counting QRS complexes over a known time gives the heart rate, and the time between two neighbouring R peaks is the length of one cycle (Example 15.3). 44The atria also repolarise, but their small signal falls during the much larger QRS complex and is hidden in it. Doctors read an ECG the way you spot a typo in a familiar word: healthy hearts recorded with the same electrode positions give traces of very similar shape, so a wave that is too tall, too wide, missing or out of place stands out as a sign of possible trouble, such as damaged heart muscle or a fault in the conducting pathway.

15.4 Double Circulation

Arteries carry blood away from the heart and veins bring it back. Cut across either and you see a wall of three coats (Fig. 15.15):

• tunica intima: the inner lining, a single sheet of flat (squamous) endothelial cells;
• tunica media: the middle coat, built of smooth muscle together with elastic fibres;
• tunica externa: the outer coat, fibrous connective tissue rich in collagen fibres.

Compare the two and the middle coat makes the difference: it is far thinner in a vein than in an artery. That fits their jobs. An artery takes the full force of each ventricular push and must stretch and spring back, while blood in a vein returns under low pressure. Capillaries, which connect the smallest arteries to the smallest veins, have walls of endothelium alone, which is why exchange with the tissues happens there.

Now follow a single red cell on one complete trip (Fig. 15.16). It leaves the right ventricle short of oxygen and travels along the pulmonary artery to the lungs. In a lung capillary it unloads carbon dioxide and loads oxygen in less than a second, then rides the pulmonary veins back to the left atrium. That first lap, right ventricle to left atrium, is the pulmonary circulation.

Next the left ventricle fires it into the aorta. The aorta divides into arteries, the arteries into arterioles and the arterioles into capillaries, where our red cell finally reaches a tissue: oxygen, nutrients and other supplies go out, carbon dioxide and wastes come in. Collected by venules, then veins, then one of the two venae cavae, it re-enters the heart at the right atrium. This second lap, left ventricle to right atrium, is the systemic circulation. Two laps mean two passes through the heart per trip, so the arrangement is called double circulation (दोहरा परिसंचरण).

Keeping the two loops apart has two benefits. Tissues always receive fully oxygenated blood, which the active muscles and warm bodies of mammals need. And each loop can run at its own pressure: the left ventricle drives blood around the whole body at high pressure, while the right ventricle sends it through the delicate lungs at a much lower pressure.

Two special routes are worth knowing. Blood leaving the stomach and intestine does not return straight to the heart. The hepatic portal vein takes it to the liver first, so that absorbed nutrients and harmful substances pass through the liver before the blood joins the systemic circulation; this link is the hepatic portal system. (A portal vein starts in the capillaries of one organ and ends in the capillaries of another.) The heart draws almost nothing from the blood rushing through its chambers: its muscle is fed by its own coronary system of vessels, with coronary arteries branching off the base of the aorta and coronary veins draining back into the right atrium.

15.5 Regulation of Cardiac Activity

A frog's heart removed from the body keeps beating for some time in a dish of suitable salt solution, with every nerve cut. A transplanted human heart is not reconnected to the recipient's nerves, yet it beats for years. The beat must therefore start inside the heart, in its nodal tissue. The heart regulates its own normal activity, so it is called myogenic (beat started by muscle).

The brain can still turn the rhythm up or down. A control centre in the medulla oblongata, the lowest part of the brain, sends instructions through the two branches of the autonomic nervous system (ANS), and hormones add a third input (Fig. 15.17, Table 15.6).

15.6 Disorders of Circulatory System

Blood pressure is the push of blood against the walls of the arteries, measured in millimetres of mercury (mm Hg). A reading such as 120/80, said '120 over 80', has two parts. The first, systolic pressure, is the peak reached as the ventricles pump; the second, diastolic pressure, is the lowest value, while the ventricles rest. A reading of 120/80 is taken as normal.

High blood pressure (hypertension) means pressure that stays above normal: if readings taken on several occasions stay at 140/90 or above, the person has hypertension. It often causes no symptoms for years, yet it overworks the heart and damages the arteries, leading to heart disease, and over time it can harm the brain (strokes) and the kidneys too.

In coronary artery disease (CAD) the trouble lies in the coronary arteries themselves. Over many years, deposits of fat and cholesterol, together with calcium and fibrous tissue, build up in their walls as plaque. This process, atherosclerosis (a name NCERT also uses for CAD), stiffens the arteries and narrows their lumen, so less blood can reach the heart muscle (Fig. 15.18).

Narrowed arteries may supply enough blood while you sit, but not when you climb stairs in a hurry. The heart muscle then runs short of oxygen and signals it with sudden, acute chest pain, often spreading to the left arm or jaw: angina (angina pectoris). Any condition that cuts blood flow to the heart muscle can cause it. Angina can occur at any age and in both men and women, but it becomes more common from middle age on.

People often use 'heart failure', 'heart attack' and 'cardiac arrest' as if they meant the same thing; they do not (the comparison below). In heart failure the heart keeps beating but pumps too weakly to meet the body's needs, so blood dams up in the veins behind it. Fluid collecting in the lungs (congestion) makes the person breathless, hence the fuller name congestive heart failure. A heart attack is sudden damage to part of the heart muscle when its blood supply is cut off, usually by a clot in a narrowed coronary artery. In cardiac arrest the heart stops beating effectively altogether.