The Cardiovascular System: Blood, Heart, Vessels and Circulation

1Overview

A resting heart beats about once a second, and with each beat it must push blood to the toes and back. In a lifetime it contracts billions of times without a rest. The cardiovascular system, a pump, a network of tubes and a fluid tissue, delivers oxygen and nutrients, removes wastes, carries hormones and heat, and plays a role in defence and in pH and temperature control. This lesson treats the blood, the heart, the blood vessels, the regulation of blood pressure and the clotting mechanism, and ends with the system's links to other systems and to disease.

2Blood: a fluid connective tissue

Blood is a connective tissue with formed elements suspended in a liquid matrix, plasma. It makes up about 8% of body weight (roughly 5 to 6 L in males and 4 to 5 L in females) and is slightly alkaline, with a pH near 7.4 (normal 7.35 to 7.45) and a viscosity about five times that of water. Its three functions are transport (oxygen, CO₂, nutrients, wastes, hormones), defence (white cells, and platelets with plasma proteins that plug breaks) and homeostasis (redistributing heat between the core and the skin, buffering pH, and regulating the water content of cells).

Hematocrit, the percentage of blood volume occupied by red cells, is about 45% on average (males about 42 to 52%, females about 37 to 47%). In a centrifuged tube the red cells settle at the bottom, a thin "buffy coat" of white cells and platelets sits above them (under 1%), and plasma is on top.

3The heart: structure and circulation

The heart is a fist-sized muscular pump sitting in the mediastinum between the lungs, enclosed in a sac, the pericardium, whose slippery fluid reduces friction. The wall has three layers: the outer epicardium, the thick myocardium of cardiac muscle, and the inner endocardium that lines the chambers and valves.

The heart has four chambers. The two atria receive blood and the two ventricles pump it out. The right atrium receives lower-oxygen blood from the superior and inferior venae cavae and the coronary sinus; the right ventricle pumps it to the lungs. The left atrium receives oxygen-rich blood from the pulmonary veins; the left ventricle pumps it to the body and has a much thicker wall because it works against higher resistance.

The atrioventricular valves are anchored by cords (chordae tendineae) to papillary muscles so that they do not flip back. Two circuits result. The pulmonary circuit runs from the right ventricle to the lungs and back to the left atrium. The systemic circuit runs from the left ventricle through the aorta to the tissues and back to the right atrium. The heart muscle itself is fed by the coronary arteries, which arise just above the aortic valve. Flow in them is greatest when the heart relaxes. Because there are few connections between branches, a blocked branch can cause a myocardial infarction (heart attack).

4Electrical activity and the cardiac cycle

Cardiac muscle is autorhythmic: it generates its own impulses. About 1% of heart cells are specialized conducting cells; the other 99% are contractile cells. The impulse follows a fixed route.

1. The SA node in the right atrium has the highest rate of spontaneous depolarization and sets the pace (the sinus rhythm).
2. The impulse spreads across both atria in about 50 ms, which contract.
3. At the AV node the impulse is delayed about 100 ms, giving the atria time to finish emptying into the ventricles.
4. It passes down the bundle of His and the left and right bundle branches in the interventricular septum.
5. Purkinje fibers spread it through the ventricular muscle, so contraction starts at the apex and moves toward the base, squeezing blood upward toward the arteries.

The pacemaker cells have no stable resting potential: a slow Na⁺ leak raises the voltage to threshold, Ca²⁺ drives depolarization and K⁺ leaving repolarizes the cell. Contractile cells show a long plateau of slow Ca²⁺ entry, so one action potential lasts 250 to 300 ms. The long refractory period prevents tetanus and lets the heart relax and refill between beats. If the SA node fails, lower sites take over at slower intrinsic rates (AV node 40 to 60 beats per minute, ventricular Purkinje fibers 15 to 20).

An electrocardiogram (ECG) records this electrical activity from the skin. The P wave is atrial depolarization, the QRS complex is ventricular depolarization (large because of the ventricles' mass; atrial repolarization is hidden within it) and the T wave is ventricular repolarization. A long PR interval indicates delayed conduction from the SA node to the ventricles, and heart blocks are graded from first degree (delay) to third degree (no relation between P waves and QRS complexes).

The cardiac cycle

Systole is contraction and diastole is relaxation. Blood always moves from higher to lower pressure.

1. Ventricular filling. In diastole the AV valves are open and about 70 to 80% of ventricular filling is passive. Atrial contraction (the "atrial kick", following the P wave) adds the remaining 20 to 30%.
2. Isovolumic contraction. Ventricular pressure rises and closes the AV valves; all valves are shut, so volume does not change.
3. Ejection. Ventricular pressure exceeds arterial pressure, the semilunar valves open and blood is ejected. The stroke volume is about 70 to 80 mL per beat, from end-diastolic volume of about 130 mL, leaving about 50 to 60 mL (end-systolic volume).
4. Isovolumic relaxation. Pressure falls and the semilunar valves close, producing a small notch on pressure tracings.
5. When ventricular pressure falls below atrial pressure the AV valves open and filling resumes.

The "lub-dub" heart sounds come from valve closure: S1 is the AV valves closing at the start of ventricular systole and S2 is the semilunar valves closing at the start of ventricular diastole. Turbulent flow through a damaged valve produces a murmur.

5Cardiac output and its control

Cardiac output (CO) is the volume pumped by each ventricle per minute: CO = heart rate (HR) × stroke volume (SV). At rest a typical adult has an SV of about 70 mL and an HR of about 75 beats per minute, giving about 5.25 L per minute; during exercise in healthy young people both rise, and CO can reach roughly 19.5 L per minute.

• Heart rate is set by the autonomic nervous system. The cardioaccelerator centre in the medulla (sympathetic, norepinephrine) speeds the heart; the cardioinhibitory centre (vagus nerve, acetylcholine) slows it. At rest the vagus keeps the rate well below the SA node's intrinsic rate (about 100 beats per minute). Epinephrine, thyroid hormones and caffeine raise it.
• Stroke volume depends on three factors. Preload is the stretch of the ventricle at the end of filling; by the Frank-Starling principle, the force of contraction is proportional to the initial length of the muscle fiber. Contractility is the force of contraction (increased by sympathetic stimulation and epinephrine). Afterload is the resistance the ventricle must overcome; high vascular resistance or a damaged valve increases it and reduces SV.

6Blood vessels, blood pressure and capillary exchange

Vessels form a closed system: arteries carry blood away from the heart, arterioles and capillaries distribute it and veins return it. Arteries and veins have three layers: the tunica intima (a lining of endothelium), the tunica media (smooth muscle and elastic fibres, thickest in arteries) and the tunica externa (collagen that anchors the vessel).

In a capillary bed, precapillary sphincters open when tissues need oxygen or have excess waste and close when tissues are at rest, so blood is directed to active organs such as working muscle or a digesting intestine.

Blood pressure

Blood pressure is the force that blood exerts on vessel walls, normally measured in mm Hg at the brachial artery. A normal reading is about 120/80: systolic pressure (about 120) from ventricular contraction over diastolic pressure (about 80) from relaxation. Pulse pressure is the difference (about 40 mm Hg), and mean arterial pressure (MAP), the average pressure driving blood into tissues, is estimated as diastolic + one third of the pulse pressure (about 93 mm Hg for 120/80). A sustained MAP below about 60 mm Hg deprives tissues of oxygen and especially harms neurons.

Flow depends on pressure and resistance. Resistance increases with vessel length and blood viscosity and decreases sharply with vessel radius (to the fourth power): halving the radius raises resistance 16-fold. Because radius is the only factor that changes quickly, vasoconstriction and vasodilation of arterioles are the main way pressure and flow are adjusted. Blood pressure also increases with higher cardiac output, greater blood volume and stiffer arteries.

Venous return needs a boost because venous pressure is low. The skeletal muscle pump squeezes veins and valves force blood toward the heart; the respiratory pump draws blood into the chest as thoracic pressure falls during inhalation; and venoconstriction, driven by sympathetic nerves, moves blood out of reserves. Standing still for a long time lets blood pool in the legs, and defective valves cause varicose veins.

Capillary exchange

Gases and small lipid-soluble molecules diffuse directly through capillary walls, glucose and ions use transporters or clefts, and water moves by osmosis (Lesson 3). Bulk flow of fluid is driven by pressure.

Capillary hydrostatic pressure (CHP) falls from about 35 mm Hg at the arterial end to about 18 mm Hg at the venous end. Blood colloid osmotic pressure (BCOP), produced by plasma proteins, which cannot cross the capillary wall, stays near 25 mm Hg. Net filtration pressure equals CHP minus BCOP, so it is about +10 mm Hg at the arterial end (fluid leaves) and about -7 mm Hg at the venous end (fluid returns). A few litres per day are not reabsorbed and are returned by the lymphatic system.

7Hemostasis: stopping bleeding

When a vessel is damaged three overlapping steps limit blood loss.

1. Vascular spasm. Smooth muscle in the wall contracts, triggered by endothelins and pain receptors, narrowing the vessel for up to about 30 minutes.
2. Platelet plug. Platelets stick to exposed collagen and clump. They release ADP, which recruits more platelets, and serotonin and prostaglandins, which maintain vasoconstriction.
3. Coagulation. A cascade of clotting factors, in which each activated factor activates the next, ends in the common pathway: factor X activates prothrombin to thrombin, and thrombin converts soluble fibrinogen into insoluble fibrin threads that form a mesh trapping blood cells. Calcium and vitamin K are required; the liver makes most clotting factors.

The platelet recruitment and the cascade are a form of positive feedback (Lesson 3): each step stimulates more clotting, until the injury is sealed. It is kept local by plasma anticoagulants such as antithrombin and heparin. Afterward, the clot retracts, and the enzyme plasmin breaks down fibrin (fibrinolysis) so the vessel can reopen.

Aspirin inhibits platelet aggregation and thrombolytic drugs break up clots; the latter work best within hours of a stroke caused by a clot, after bleeding has been ruled out.

8Homeostasis, interdependence and disease

Blood pressure is controlled by negative feedback. Baroreceptors in the aorta and carotid sinuses detect stretch and signal the medulla. If pressure rises, the medulla increases vagal output and reduces sympathetic output, slowing the heart and dilating vessels; if pressure falls, the opposite occurs. Slower, hormonal mechanisms add to this: the kidney's renin-angiotensin-aldosterone system and ADH conserve water and constrict vessels, and atrial natriuretic hormone from the stretched atria promotes sodium and water loss (Lesson 12). The cardiovascular system also depends on the others: the respiratory system loads oxygen, the digestive system supplies nutrients, the urinary system adjusts blood volume, and the lymphatic system returns fluid.

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