Learn — Cardiovascular system

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Longest vein — great saphenous

The great (long) saphenous vein is the longest vein in the body, running the whole length of the limb from the medial end of the dorsal venous arch of the foot to the femoral vein in the groin. It matters far beyond the examination hall because it is the vein of the emergency venous cut-down, the conduit harvested for coronary and peripheral bypass grafts, and the vein whose incompetent valves produce varicose veins and the venous ulcer above the medial malleolus.

It begins at the medial end of the dorsal venous arch of the foot, passes about 2 cm in front of the medial malleolus, ascends the medial side of the leg with the saphenous nerve, crosses about a hand's breadth behind the medial border of the patella at the knee and runs up the medial side of the thigh.
It ends by piercing the cribriform fascia over the saphenous opening, about 3 to 4 cm below and lateral to the pubic tubercle, and drains into the femoral vein at the saphenofemoral junction.
Its named tributaries at that junction — the superficial epigastric, superficial circumflex iliac and superficial and deep external pudendal veins, together with the accessory saphenous veins — must all be ligated at surgery, because a missed tributary is the classic reason varicose veins recur.
It carries between 10 and 20 valves, more in the leg than in the thigh, and communicates with the deep veins through perforating veins whose valves normally allow flow only from superficial to deep; incompetence of those valves is what produces varicose veins, and it is why a reversed segment must be used for a bypass graft.
The saphenous nerve, the largest cutaneous branch of the femoral nerve (L3 and L4), accompanies the vein below the knee, so stripping or repeated cannulation there causes numbness or burning along the medial side of the leg and foot.
The small (short) saphenous vein is the contrast to learn with it: it begins at the lateral end of the dorsal venous arch, passes behind the lateral malleolus with the sural nerve, ascends the back of the calf and ends in the popliteal vein in the popliteal fossa.
Because its position 2 cm in front of the medial malleolus is constant in every patient, however shocked, obese or oedematous, it is the classical site for a venous cut-down when no peripheral vein can be found.
The chronic venous picture in the leg is diagnostic: varicosities on the medial calf, ankle oedema that is worse at the end of the day, haemosiderin pigmentation and lipodermatosclerosis in the gaiter area, and a shallow, exudative ulcer just above the medial malleolus.
The Trendelenburg test localises the leak: with the leg elevated and emptied and a tourniquet at the saphenofemoral junction, rapid filling while the tourniquet stays on means incompetent perforators, and filling only on releasing it means saphenofemoral incompetence.

Arterial supply of lung

The lung has a double arterial supply: the pulmonary arteries bring the whole cardiac output of deoxygenated blood from the right ventricle for gas exchange, while the small bronchial arteries bring oxygenated blood from the aorta to nourish the airways and supporting tissue. The two systems differ completely in pressure, and that difference explains both why a pulmonary embolus often does not infarct the lung and why haemoptysis can be torrential.

The pulmonary trunk leaves the right ventricle and divides at about the level of the sternal angle (T4 to T5) into the right and left pulmonary arteries, carrying deoxygenated blood — the only arteries in the adult that do so.
The right pulmonary artery is longer and more horizontal and passes behind the ascending aorta and the superior vena cava to reach the right hilum.
At the hilum the relation of the pulmonary artery to the bronchus is remembered as RALS: on the Right it is Anterior, on the Left it is Superior; the pulmonary veins are the most anterior and inferior structures on both sides.
The bronchial arteries are usually one on the right, from the third posterior intercostal artery, and two on the left arising directly from the descending thoracic aorta at about T5 to T6; together they carry only about 1 to 2 per cent of the cardiac output.
Bronchial arteries supply the bronchial tree down to the respiratory bronchiole, the visceral pleura, the walls of the pulmonary vessels and the hilar lymph nodes; beyond the respiratory bronchiole the tissue is nourished directly from alveolar gas and pulmonary blood.
Bronchial venous blood returns partly to the azygos and hemiazygos veins and partly into the pulmonary veins; that second stream is deoxygenated blood reaching the left atrium, the physiological shunt of about 2 per cent that keeps arterial oxygen just below alveolar oxygen.
The pulmonary circulation is a low-pressure, low-resistance, high-compliance system: the pulmonary artery pressure is about 25/8 mmHg with a mean near 15 mmHg and the pulmonary capillary wedge pressure is 6 to 12 mmHg, against a systemic mean of about 90 mmHg.
Hypoxia constricts pulmonary vessels, the opposite of the systemic response, which diverts blood away from poorly ventilated alveoli; when the hypoxia is global, as in chronic lung disease or at altitude, this raises pulmonary artery pressure and eventually causes cor pulmonale.
Because of the dual supply, an embolus in a pulmonary artery causes frank infarction in only a minority of patients, usually those whose bronchial circulation is already compromised by heart or lung disease.

Heart anatomy

The heart is a four-chambered muscular pump that lies obliquely in the middle mediastinum inside the pericardium, with about two-thirds of its bulk to the left of the midline and its apex reaching the fifth left intercostal space in the midclavicular line. The right side receives systemic venous blood and pumps it to the lungs at low pressure, the left side receives oxygenated blood and pumps it to the body at high pressure, and every valve area, ECG lead position and coronary territory a nurse uses is read off this surface anatomy.

Chambers and surfaces: the right atrium forms the right border, the right ventricle most of the anterior surface and the inferior border, the left ventricle the left border and apex, and the left atrium the base of the heart lying most posteriorly against the oesophagus.
The left ventricular wall is roughly three times as thick as the right (about 8 to 12 mm against 3 to 5 mm) because it works against systemic rather than pulmonary resistance; the wall itself is endocardium, myocardium and epicardium, which is the visceral layer of serous pericardium.
Auscultation areas do not lie over their valves: aortic at the second right intercostal space beside the sternum, pulmonary at the second left, tricuspid at the lower left sternal border in the fourth or fifth space, and mitral at the apex in the fifth left intercostal space in the midclavicular line.
The coronary arteries arise from the aortic sinuses just above the aortic valve. The left coronary artery divides into the anterior interventricular (left anterior descending) and circumflex branches, and the right coronary artery gives the right marginal branch and, in about 85 per cent of people, the posterior interventricular branch.
The left anterior descending artery supplies the anterior wall of the left ventricle and the anterior two-thirds of the interventricular septum, which is why its occlusion is called the widow-maker and shows ST elevation in leads V1 to V4.
The right coronary artery supplies the sinuatrial node in about 60 per cent of hearts and the atrioventricular node in about 80 to 90 per cent, so an inferior myocardial infarction from a right coronary occlusion characteristically brings bradycardia and heart block.
The coronary arteries fill during diastole, not systole, because systolic myocardial compression squeezes them shut; any tachycardia shortens diastole and worsens ischaemia.
The pericardium is a tough outer fibrous sac fused to the central tendon of the diaphragm plus an inner serous sac whose two layers are separated by about 15 to 50 mL of fluid; because the fibrous layer cannot stretch acutely, a rapid collection of even 100 to 200 mL can tamponade the heart, while a slow effusion may reach a litre without doing so.
The fibrous skeleton of the heart electrically insulates the atria from the ventricles, so the atrioventricular bundle is the only normal conducting path between them.

Heart sounds S1-S4

The heart sounds are the short noises made when the valves shut and when blood rushes into a ventricle, and they divide the cardiac cycle into systole and diastole for anyone with a stethoscope. S1 and S2 are normal in everyone and mark the beginning and end of systole, while S3 and S4 are low-pitched filling sounds that are sometimes normal and often the first bedside sign of a failing or a stiff ventricle.

S1 is the closure of the mitral and then the tricuspid valve at the start of ventricular systole; it is low-pitched and long, heard best at the apex, described as lub, and it coincides with the carotid upstroke, which is how you tell systole from diastole when the rate is fast.
S2 is the closure of the aortic and then the pulmonary valve at the end of systole; it is higher-pitched and shorter, heard best at the base, described as dub, and it splits physiologically on inspiration because increased venous return delays pulmonary valve closure.
Abnormal splitting of S2 is diagnostic: a wide fixed split that does not vary with respiration is an atrial septal defect, and reversed or paradoxical splitting, in which the split widens on expiration, points to left bundle branch block or severe aortic stenosis.
S1 is loud in mitral stenosis, tachycardia and a short PR interval and soft in mitral regurgitation, a long PR interval and poor left ventricular function; A2 is loud in systemic hypertension and P2 is loud in pulmonary hypertension.
S3 is a low-pitched sound in early diastole caused by rapid passive filling striking a compliant or overloaded ventricle; it can be normal under the age of about 40 and in pregnancy and athletes, but in an older or breathless patient it is a ventricular gallop that means volume overload or heart failure.
S4 is a low-pitched sound in late diastole produced by atrial contraction against a stiff, non-compliant ventricle; it is heard in left ventricular hypertrophy, long-standing hypertension, aortic stenosis, ischaemia and hypertrophic cardiomyopathy, and it cannot occur in atrial fibrillation because there is no coordinated atrial contraction.
Both extra sounds together with a tachycardia merge into a summation gallop; a pericardial friction rub, by contrast, is a scratchy to-and-fro sound heard best with the patient sitting forward in expiration.
Technique decides what you hear: the diaphragm picks up high-pitched sounds such as S1, S2 and regurgitant murmurs, while the bell held lightly at the apex with the patient in the left lateral position is what brings out the low-pitched S3, S4 and the rumble of mitral stenosis.

Cardiac output (CO = HR x SV)

Cardiac output is the volume of blood the left ventricle ejects in one minute, and it is the product of heart rate and stroke volume, so at a heart rate of about 72 beats per minute and a stroke volume of about 70 mL it comes to roughly 5 litres per minute in a resting adult. It is the single number that decides whether tissues are perfused, which is why every drug, every fluid bolus and every arrhythmia on a ward is judged by what it does to heart rate or to stroke volume.

Cardiac output equals heart rate multiplied by stroke volume; the resting adult value is about 4.5 to 5 litres per minute and it can rise to 20 to 25 litres per minute in heavy exercise and higher still in a trained athlete.
Cardiac index is cardiac output divided by body surface area and normally lies between about 2.5 and 4.0 litres per minute per square metre; it is used instead of raw output so that a small woman and a large man can be compared.
Stroke volume is normally about 70 mL (60 to 80 mL) and is set by three things: preload, which is end-diastolic volume acting through the Frank-Starling mechanism, afterload, which is the resistance the ventricle ejects against, and contractility, the intrinsic force of the myocardium.
Mean arterial pressure equals cardiac output multiplied by systemic vascular resistance, and mean arterial pressure can be estimated at the bedside as the diastolic pressure plus one-third of the pulse pressure; a mean of at least 65 mmHg is the usual target for organ perfusion.
Raising the heart rate raises output only up to a point: beyond roughly 160 to 180 beats per minute diastole becomes too short to fill the ventricle or to perfuse the coronary arteries, so output falls even though the rate is higher.
Cardiac output rises physiologically in exercise, fever, anxiety, anaemia, hyperthyroidism and pregnancy, where it increases by about 30 to 50 per cent and peaks in the late second trimester; it falls in myocardial infarction, arrhythmia, hypovolaemia, valve disease, tamponade and with beta blockers.
In the steady state venous return must equal cardiac output, which is why anything that obstructs venous return, such as tamponade, tension pneumothorax or the supine hypotensive syndrome of late pregnancy, drops the output at once.
Cardiac output is measured clinically by thermodilution through a pulmonary artery catheter, by echocardiography or from the arterial pressure waveform, and the Fick principle expresses it as oxygen consumption divided by the arteriovenous oxygen difference.

Blood pressure regulation

Arterial blood pressure is the product of cardiac output and systemic vascular resistance, and the body defends it with three sets of controls working over three different time scales. Nervous reflexes act within seconds, hormones act over minutes to hours, and the kidney sets the long-term level by deciding how much sodium and water stay in the body, which is why almost every antihypertensive drug works on one of those three systems.

Blood pressure equals cardiac output multiplied by systemic vascular resistance, so anything that changes heart rate, stroke volume or arteriolar tone changes the pressure; mean arterial pressure can be estimated as diastolic pressure plus one-third of the pulse pressure.
Second-to-second control is the baroreceptor reflex from stretch receptors in the carotid sinus (afferent in the glossopharyngeal nerve) and the aortic arch (afferent in the vagus); a rise in pressure increases their firing, inhibits the vasomotor centre in the medulla and produces vasodilatation with bradycardia, and the reflex is most sensitive between about 60 and 180 mmHg.
The baroreceptors reset within a day or two to whatever pressure they are exposed to, which is why they buffer sudden changes such as standing up but never correct established hypertension.
Peripheral chemoreceptors in the carotid and aortic bodies fire when the arterial oxygen tension falls below about 60 mmHg or carbon dioxide rises, and they raise pressure by sympathetic vasoconstriction; the central nervous system ischaemic response is the last-ditch reflex that produces an intense pressor response when cerebral perfusion is severely reduced.
The renin-angiotensin-aldosterone system is the main hormonal control. Renin is released by juxtaglomerular cells when renal perfusion pressure falls, when sodium chloride at the macula densa falls or when beta-1 sympathetic activity rises, and it converts angiotensinogen from the liver into angiotensin I, which angiotensin-converting enzyme in the pulmonary endothelium converts to angiotensin II.
Angiotensin II raises pressure five ways: direct arteriolar vasoconstriction, aldosterone release from the zona glomerulosa causing sodium and water retention with potassium loss in the collecting duct, antidiuretic hormone release, thirst, and enhanced proximal tubular sodium reabsorption; ACE inhibitors and angiotensin receptor blockers work here.
Antidiuretic hormone from the posterior pituitary retains water through V2 receptors in the collecting duct and constricts vessels through V1 receptors at high concentration, while atrial natriuretic peptide, released when the atria are stretched, does the opposite by causing natriuresis and vasodilatation.
Long-term control belongs to the kidney through pressure natriuresis: a rise in arterial pressure increases sodium and water excretion until blood volume and pressure fall back, a mechanism with effectively infinite gain, which is why sustained hypertension always involves a shifted renal pressure-natriuresis curve.
Hypertension is conventionally diagnosed at a persistent 140/90 mmHg or more on repeated measurement in Indian and WHO practice, while the American guideline moved the threshold to 130/80 mmHg in 2017 and kept it in its 2025 update; orthostatic hypotension is a fall of at least 20 mmHg systolic or 10 mmHg diastolic within three minutes of standing.

SA node — pacemaker

The sinuatrial node, also called the node of Keith and Flack, is a small crescent of specialised cardiac muscle lying just beneath the epicardium in the upper part of the right atrium, at the junction of the superior vena cava with the atrium at the upper end of the crista terminalis. It is the pacemaker of the heart because it depolarises spontaneously faster than any other cardiac tissue, so it captures the whole conducting system and sets the rhythm that the ECG records as a sinus P wave.

The sinuatrial node lies at the junction of the superior vena cava and the right atrium and is supplied by the sinuatrial nodal artery, a branch of the right coronary artery in about 60 per cent of hearts and of the left circumflex artery in the rest.
Its intrinsic discharge rate is about 60 to 100 impulses per minute; the atrioventricular node and the junctional tissue take over at about 40 to 60 and the bundle of His, bundle branches and Purkinje fibres at about 20 to 40, so the slower a pacemaker sits in the chain, the slower the escape rhythm it produces.
Nodal cells have no stable resting potential; a funny sodium current makes the membrane drift up from about minus 60 mV to threshold, and the upstroke is carried by calcium entering through T-type and then L-type channels, not by fast sodium channels, which is why calcium channel blockers slow the node.
The impulse spreads through the atria and by internodal tracts and Bachmann's bundle to the left atrium, reaches the atrioventricular node where it is delayed by about 0.1 second, and then travels down the bundle of His to the bundle branches and Purkinje network.
That atrioventricular delay is the PR interval on the ECG, normally 0.12 to 0.20 seconds, and it exists so that the atria can finish emptying before the ventricles contract; the atrial kick it protects contributes roughly a fifth to a third of ventricular filling and is lost in atrial fibrillation.
Conduction is slowest at the atrioventricular node and fastest in the Purkinje fibres, which is what allows the two ventricles to contract almost simultaneously from the apex upwards.
The vagus nerve slows the node through acetylcholine at M2 receptors and the sympathetic nerves speed it through beta-1 receptors and adrenaline; vagal manoeuvres such as carotid sinus massage and the Valsalva manoeuvre exploit this, and atropine blocks it, which is why atropine is the first drug in symptomatic bradycardia.
When the node fails, the picture is sick sinus syndrome with sinus bradycardia, sinus pauses or alternating bradycardia and tachycardia, and the definitive treatment is a permanent pacemaker.

Stroke volume

Stroke volume is the amount of blood one ventricle ejects with a single beat, and it is the difference between the end-diastolic volume and the end-systolic volume, normally about 70 mL from a filled volume of roughly 120 mL. It is the variable that both the heart and the nurse can actually change, because it is set by preload, afterload and contractility, and it is what falls first in haemorrhage, tamponade and heart failure while the heart rate rises to hide it.

Stroke volume equals end-diastolic volume minus end-systolic volume; with an end-diastolic volume of about 120 mL and an end-systolic volume of about 50 mL the stroke volume is about 70 mL, and roughly 40 to 50 mL is left behind in the ventricle after every beat.
Ejection fraction is stroke volume divided by end-diastolic volume, normally 55 to 70 per cent; below 40 per cent is heart failure with reduced ejection fraction, and it is the number quoted from every echocardiogram.
Preload is the end-diastolic volume or fibre length, and the Frank-Starling law states that the greater the stretch of the myocardial fibre in diastole, the more forcefully it contracts, so a rise in venous return automatically raises stroke volume beat by beat.
The Starling curve has a peak: a normal ventricle keeps climbing with volume, but a failing or overstretched one plateaus and then falls, which is why a fluid bolus that helps a dehydrated patient can drown a patient in heart failure.
Afterload is the resistance against which the ventricle ejects, chiefly aortic pressure and systemic vascular resistance; raising it lowers stroke volume, which is exactly how vasodilators, ACE inhibitors and nitrates improve output in a failing heart.
Contractility is the force of contraction at a given fibre length. It is increased by sympathetic stimulation, circulating catecholamines, dobutamine, digoxin and calcium, and decreased by hypoxia, acidosis, hyperkalaemia, myocardial infarction, beta blockers and calcium channel blockers.
Atrial contraction adds about a fifth to a third of the end-diastolic volume, so losing the atrial kick in atrial fibrillation, or losing filling time in a tachycardia above roughly 160 beats per minute, cuts stroke volume even when the ventricle itself is normal.
Pulse pressure, the systolic minus the diastolic pressure and normally about 40 mmHg, tracks stroke volume at the bedside: a narrowing pulse pressure with a rising heart rate is early hypovolaemia long before the systolic pressure falls.
Anything that obstructs filling drops stroke volume immediately: haemorrhage, dehydration, cardiac tamponade, tension pneumothorax, high positive end-expiratory pressure and aortocaval compression by the pregnant uterus.

Arterioles vs veins — diameter, resistance

The vessels of the circulation are specialised by wall structure into elastic arteries that smooth the pulse, muscular arteries that distribute, arterioles that resist, capillaries that exchange and veins that store. The two ends of that list matter most in practice: arterioles are the resistance vessels that set blood pressure, and veins are the capacitance vessels that hold most of the blood volume in reserve.

Arterioles have a small lumen and a thick coat of smooth muscle relative to that lumen, so they generate the greatest resistance and show the steepest fall in pressure of any segment, taking the mean pressure down from roughly 85 to 90 mmHg to about 30 to 35 mmHg by the start of the capillary.
Resistance varies inversely with the fourth power of the radius, so halving the radius of an arteriole raises its resistance about sixteen-fold; that is why a small change in arteriolar tone changes blood pressure so much and why alpha-1 constriction and beta-2 dilatation are such powerful drug targets.
Capillaries are a single layer of endothelium on a basement membrane, about 5 to 10 micrometres wide, and they carry the largest total cross-sectional area in the body, so blood velocity there is slowest, which is exactly what exchange needs.
Capillaries come in three structural types: continuous (muscle, skin, brain, where tight junctions make the blood-brain barrier), fenestrated (renal glomerulus, intestinal villi, endocrine glands) and sinusoidal or discontinuous (liver, spleen, bone marrow).
Veins have thin walls, wide lumens and low pressure, falling from about 15 to 20 mmHg in venules to nearly zero at the right atrium; they act as capacitance vessels and at rest hold roughly 60 to 70 per cent of the total blood volume.
Limb veins, and especially the veins of the lower limb, contain semilunar valves that make flow one-way towards the heart; the venae cavae, the dural venous sinuses, the pulmonary veins and the portal system have no valves, and incompetent valves in the leg produce varicose veins and venous ulcers.
Venous return depends on the skeletal muscle pump, the respiratory pump, venoconstriction and gravity rather than on the venous pressure alone, which is why immobility, a full cast or prolonged standing all reduce it.
The aorta and the large elastic arteries act as a windkessel, expanding in systole and recoiling in diastole so that flow to the tissues continues between beats and diastolic pressure is maintained for coronary filling; stiffening of these vessels with age is what widens pulse pressure in the elderly.

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