Cardiovascular
The cardiovascular system is a pump and a plumbing network that never rests. When one small part fails, the trouble spreads everywhere. This chapter starts with the pressure inside the pipes and ends with the muscle of the pump itself. You will cover hypertension, coronary disease and heart attack, heart failure, valve problems, the rhythms on the EKG, and the diseases of the peripheral vessels.
By the end of this chapter you can
- Explain what sets blood pressure, and how hypertension damages organs.
- Tell stable angina apart from a myocardial infarction, and name its markers.
- Compare left- and right-sided failure, and systolic with diastolic heart failure.
- Tell valve stenosis from regurgitation.
- Read the basic EKG waves. Spot dangerous arrhythmias and peripheral vascular disease.
Section 1Blood pressure & hypertension
Every time your heart beats, it pushes blood against the walls of your arteries. Blood pressure is the force of that push. We write it as two numbers, like 120/80 mmHg. The top number (systolic) is the pressure while the heart squeezes. The bottom number (diastolic) is the pressure while the heart relaxes between beats. Healthy pressure keeps blood moving to every organ. It does that without pounding the vessels hard enough to damage them.
What actually sets the pressure
Two things multiply together to set your blood pressure. One is how much blood the heart pumps each minute. The other is how tight the pipes are. In textbook terms, BP = cardiac output (CO) times systemic vascular resistance (SVR). Cardiac output is heart rate times stroke volume. Stroke volume is how much blood leaves the heart with each beat. Systemic vascular resistance is how narrow or squeezed down the arterioles are. Think of a garden hose. Turn the water up, and the pressure rises. Pinch the nozzle tighter, and the pressure rises too. That is why a racing heart, extra fluid, or clamped-down vessels all push the number up.
How the body keeps it steady
Your body corrects blood pressure minute by minute and day by day. It uses two main systems.
Baroreceptors are stretch sensors in the carotid arteries and the aortic arch. When pressure drops, they feel less stretch. They tell the brainstem to speed the heart and tighten the vessels. When pressure spikes, they do the opposite. This is the fast reflex, working second by second. It is also why you may feel dizzy if you stand up too quickly. The reflex needs a moment to catch up.
The RAAS (renin-angiotensin-aldosterone system) is the slower controller for the long run. When the kidneys sense low pressure or low blood flow, they release renin. Renin starts a chain that makes angiotensin II. Angiotensin II is a powerful vasoconstrictor, so it tightens vessels and raises SVR. It also tells the adrenal glands to release aldosterone. Aldosterone tells the kidneys to hold on to sodium and water. That raises blood volume, and so it raises cardiac output. Both actions raise pressure. Many blood pressure drugs (ACE inhibitors, ARBs) work by cutting into this exact pathway.
When pressure stays too high: hypertension
Hypertension means blood pressure that stays up over time. The usual cutoff is 130/80 mmHg or higher on repeated readings. It shows up in two flavors.
| Feature | Primary (essential) | Secondary |
|---|---|---|
| How common | About 90-95% of cases | About 5-10% of cases |
| Cause | No single cause you can point to. Genes, aging, salt, weight, and stress all add up | One underlying illness you can name |
| Typical triggers | Family history, obesity, a high-sodium diet, too little activity | Kidney disease, a narrowed renal artery, pheochromocytoma, sleep apnea, certain drugs |
| Onset clue | Slow, and often starts in midlife | Sudden, very high, or hard to treat. Sometimes in young patients |
| Treatment focus | Lifestyle plus medication | Fix the cause underneath |
Primary hypertension has no single cause you can fix. It grows out of genes, aging vessels, a lot of sodium, and often extra weight. Secondary hypertension is driven by one specific problem you can name. Treat that problem, and the high pressure can actually go away.
The silent killer and its targets
Hypertension has earned the nickname the silent killer. It usually causes no symptoms for years. There is no headache and no warning. The person feels fine while the high pressure quietly grinds away at organs. By the time the damage shows, it can be far along.
That damage is called target-organ damage, and it strikes the organs packed with blood vessels:
- Heart: the left ventricle must pump against higher resistance, so its wall thickens (left ventricular hypertrophy). In time it can fail. The coronary arteries also stiffen, which raises the risk of a heart attack.
- Brain: weak, pressure-battered vessels can burst or clot, which causes a stroke. Years of damage also feed vascular dementia.
- Kidneys: the tiny filtering vessels scar and narrow. That leads to chronic kidney disease, and in the end to kidney failure.
- Eyes: the vessels in the retina are a visible window onto this damage. Hypertensive retinopathy can blur or steal vision.
- Blood pressure equals cardiac output times systemic vascular resistance. More fluid, a faster heart, or tighter vessels all raise it.
- Baroreceptors correct pressure fast, moment to moment. The RAAS is slower. It tightens vessels (angiotensin II) and holds on to salt and water (aldosterone).
- Primary (essential) hypertension is 90-95% of cases and has no single cause. Secondary hypertension has a cause you can name, and often treat.
- Hypertension is the silent killer. It causes no symptoms while it quietly harms the heart, brain, kidneys, and eyes. That is target-organ damage.
- Patients feel fine, so teaching them to keep taking their drugs is critical. ACE inhibitors and ARBs work by blocking the RAAS pathway.
Section 2Coronary artery disease, angina & MI
Your heart is a muscle. Like any muscle, it needs a steady supply of oxygen-rich blood to keep working. But here is the twist. Gallons of blood rush through its chambers every hour, and the heart muscle cannot use that blood. It feeds itself through its own private plumbing, the coronary arteries. These vessels branch off the aorta and wrap around the outside of the heart. When they are open and healthy, supply keeps up with demand easily, and the muscle never notices. Trouble begins when the pipes get narrow.
How the coronary arteries get clogged
Over years, cholesterol, inflammatory cells, and cell debris build up inside the artery wall. That fatty deposit is called a plaque. This slow, silent process is atherosclerosis. As a plaque grows, it stiffens the vessel and squeezes the channel (the lumen) smaller. Less blood can get through. That is coronary artery disease (CAD). For a long time the narrowing causes no symptoms, because a resting heart does not ask for much. The problem shows up when the heart has to work harder.
Angina: the heart's cry for oxygen
Angina is chest pain or pressure caused by myocardial ischemia. Ischemia means the muscle is not getting enough oxygen for the work it is doing. It is a problem of demand versus supply. In stable angina, a fixed plaque leaves just enough room for blood flow at rest. Then the person climbs stairs, shovels snow, or gets upset. Heart rate and force climb, so oxygen demand outruns the narrowed supply. The muscle aches. The classic tip-off is that the pain is predictable. It comes on with exertion. It fades within minutes of rest or a nitroglycerin tablet, which widens vessels and eases the heart's workload. In stable angina the muscle is starved, but it is not yet dying.
Unstable angina is a different and far more dangerous animal. Here a plaque has turned fragile and has partly broken open. Pain now comes at rest, lasts longer, or is suddenly worse than the patient's usual pattern. It is one of the acute coronary syndromes (ACS). It warns you that a heart attack may be brewing.
| Feature | Stable angina | Unstable angina |
|---|---|---|
| Trigger | Exertion or stress you can predict | Often at rest, with no clear trigger |
| Plaque | Fixed, stable narrowing | Broken open and unstable |
| Relief | Rest or nitroglycerin, within minutes | Poorly relieved, and may keep going |
| Muscle status | Ischemic, meaning starved of oxygen, but not dying | At high risk. An emergency |
When the pipe closes: myocardial infarction
A myocardial infarction (MI) is a heart attack. It happens when an unstable plaque ruptures. The body treats the exposed plaque like a wound. Platelets and clotting factors rush in and build a blood clot, called a thrombus. If that clot blocks the artery all the way, blood flow stops cold. The muscle downstream is cut off from oxygen at once. The starved heart muscle begins to die within about 20 to 30 minutes, and the damage spreads over the next few hours. This is infarction, which means irreversible tissue death (necrosis). It is not the reversible starvation of angina. That is why the phrase time is muscle matters so much. Every minute the artery stays blocked, more heart is lost for good.
Recognizing an MI
The hallmark is chest pain. It is often crushing, heavy, or squeezing pressure. It may spread to the left arm, the jaw, or the back. It often comes with sweating (diaphoresis), nausea, and shortness of breath. But atypical presentations are common and easy to miss. Women, older adults, and people with diabetes may feel only fatigue, indigestion, or breathlessness. There may be no dramatic chest pain at all, because neuropathy and different symptom patterns blunt the classic warning. Three tools confirm the diagnosis:
- ECG: a STEMI (ST-elevation MI) shows a raised ST segment. That means the full thickness of the muscle is being injured by a completely blocked artery. It is a true emergency, and the vessel must be reopened right away.
- Troponin: when heart cells die, they leak the protein troponin into the blood. A rising troponin level over serial draws is the most specific sign that muscle has truly been damaged.
- The story: the pattern and timing of the pain ties it all together.
- Atherosclerosis narrows the coronary arteries over years, so less blood reaches the heart muscle. That is coronary artery disease.
- Stable angina is reversible ischemia from a demand-supply mismatch, and rest or nitroglycerin relieves it. Unstable angina comes at rest and warns of an MI to come.
- A myocardial infarction follows plaque rupture and a thrombus that blocks the artery. Muscle dies, and that death is permanent.
- Spot an MI by chest pain (watch for atypical presentations), ST-elevation on the ECG, and rising troponin. Remember that time is muscle.
Section 3Heart failure
Picture the heart as a two-sided pump that works every second of your life. The right side collects oxygen-poor blood coming back from the body and pushes it to the lungs. The left side takes freshly oxygenated blood from the lungs and drives it out to every organ. In a healthy heart, the blood coming in matches the blood going out, and tissues get just the oxygen they need. Heart failure is what happens when the pump can no longer keep up with the body's demand. It does not mean the heart has stopped. It means the heart cannot move blood forward well. Blood backs up behind the weak side, and organs downstream are left short.
Left-sided failure: the backup floods the lungs
The left ventricle is the strongest chamber, because it must push blood to the whole body. When it weakens, blood cannot move forward fast enough. It dams up behind the left side, back into the capillaries of the lungs. The rising pressure forces fluid out of those capillaries and into the air sacs. That state is pulmonary congestion, also called pulmonary edema. This is why left-sided failure is a lung story. Patients feel short of breath (dyspnea), above all with exertion. Lying flat lets fluid shift toward the lungs, so they wake up gasping or prop themselves up on pillows. Those two signs are orthopnea and paroxysmal nocturnal dyspnea. On auscultation, which just means listening to the chest, you hear crackles (rales). That is the sound of air bubbling through fluid-filled alveoli. A frothy or pink-tinged cough can appear as fluid leaks into the airways.
Right-sided failure: the backup floods the body
When the right ventricle fails, blood dams up behind it. It backs into the systemic veins that were trying to return blood to the heart. Now the congestion shows up in the body, not the lungs. Neck veins bulge under the backed-up pressure, which is jugular venous distention (JVD). Leaked fluid settles in the ankles and legs where gravity pulls it, giving peripheral edema. Blood engorges the liver and enlarges it, which is hepatomegaly. The single most common cause of right-sided failure is left-sided failure itself. Lung congestion strains the right ventricle over time. That is why untreated left failure often becomes biventricular, meaning both sides fail.
| Feature | Left-sided failure | Right-sided failure |
|---|---|---|
| Blood backs up into | Lungs (pulmonary circulation) | Body (systemic veins) |
| Hallmark signs | Dyspnea, orthopnea, crackles | JVD, peripheral edema, hepatomegaly |
| Classic complaint | Cannot breathe lying flat | Swollen legs, weight gain |
| Common cause | Hypertension, an earlier MI | Left-sided failure, lung disease |
Systolic vs diastolic: a squeeze problem or a filling problem
Failure can come from two different mechanical faults. In systolic failure, the ventricle is weak and cannot contract forcefully. It pushes out a smaller share of the blood it holds. We measure that share as the ejection fraction (EF), which here is often under 40%. Normal is usually 55 to 70%. This type is called HFrEF (heart failure with reduced ejection fraction). In diastolic failure, the squeeze is fine, but the ventricle is stiff. It cannot relax and fill properly, so less blood is there to pump even though the squeeze percentage looks normal. This type is HFpEF (preserved ejection fraction). Here is the key point. A normal EF does not rule out heart failure.
Compensation that turns against you
When cardiac output drops, the body reacts as if it were bleeding. The sympathetic nervous system fires. It speeds the heart and squeezes vessels to prop up blood pressure. The kidneys sense low flow and switch on the renin-angiotensin-aldosterone system (RAAS), which holds on to sodium and water and tightens arteries. In the short run these moves buy time. Over weeks they backfire. The extra fluid worsens the congestion. The higher pressure makes the failing heart work harder. Constant overdrive also drives ventricular remodeling, in which the heart enlarges and stiffens. This vicious cycle explains the mainstay drugs. ACE inhibitors, ARBs, and beta-blockers all work by blocking these compensations.
The stretched, overworked ventricles release B-type natriuretic peptide (BNP), a hormone that tries to make the body shed fluid. Because BNP rises when the wall is stretched, a high level is a useful marker. It points to heart failure, rather than the lungs, as the cause of shortness of breath. Explore the left- versus right-sided comparison below.
- Heart failure is a pump that cannot meet the body's demand. Blood backs up behind the failing side.
- Left-sided failure floods the lungs: dyspnea, orthopnea, crackles. Right-sided failure floods the body: JVD, peripheral edema, hepatomegaly.
- Systolic failure (HFrEF) is a weak squeeze with a low EF. Diastolic failure (HFpEF) is a stiff ventricle that fills poorly, with a normal EF.
- RAAS and sympathetic activation help at first. In time they worsen congestion and drive remodeling.
- BNP rises when the ventricle is stretched, so it helps confirm that dyspnea is coming from the heart.
Section 4Valve disorders
Picture your heart as a house with four rooms and four one-way doors between them. Those doors are your valves, and their whole job is simple. Let blood move forward, and never let it slip backward. When the heart squeezes, the doors ahead swing open easily. When it relaxes, they snap shut tight so nothing leaks back. Two of these doors do the heavy lifting on the left side of the heart, the side that pushes blood out to the whole body. The mitral valve sits between the left atrium and the left ventricle. The aortic valve sits between the left ventricle and the aorta. When a valve stops opening well, or stops sealing well, the heart has to work harder for every single beat. Over time that extra work reshapes the chamber behind it.
The two ways a valve fails: stenosis vs. regurgitation
There are really only two things that can go wrong with a door. Either it is hard to push open, or it does not shut all the way. That is the entire concept.
Stenosis means the valve has grown stiff, thick, or narrow, so the opening is too small. The chamber behind it must build much higher pressure to force blood through the tight gap. It is like trying to breathe through a pinched straw. Regurgitation means the valve does not seal, so some blood sloshes backward with each beat. It is also called insufficiency, or a leaky or incompetent valve. Now the chamber has to pump the same blood twice. It handles the normal load plus the volume that leaked back. Stenosis is mainly a pressure problem. Regurgitation is mainly a volume problem. That difference predicts how the heart changes.
| Feature | Stenosis | Regurgitation |
|---|---|---|
| Basic defect | Valve too narrow, hard to open | Valve leaks, does not close |
| Main burden | Pressure overload | Volume overload |
| Chamber response | Concentric hypertrophy (thick walls) | Eccentric hypertrophy and dilation (stretched) |
| Classic murmur timing | Systolic (aortic) or diastolic (mitral) | Depends on the valve. For example, holosystolic in MR |
The two lesions you will see most
Aortic stenosis (AS) is the classic pressure problem. The aortic door stiffens, often from calcium buildup with age (calcification). So the left ventricle must slam against a tight opening to eject blood. To make that pressure, the ventricle wall thickens (concentric hypertrophy). The classic triad you learn for symptomatic AS is angina, syncope, and dyspnea on exertion. Those symptoms often signal that the valve area has grown narrow. Patients frequently have a crescendo-decrescendo systolic murmur.
Mitral regurgitation (MR) is the classic volume problem. The mitral door does not seal. So with each squeeze, blood jets backward into the left atrium instead of only moving forward into the aorta. The left atrium and left ventricle stretch and enlarge (eccentric hypertrophy) to hold the extra volume. A holosystolic (pansystolic) murmur, heard best at the apex, is typical.
Rheumatic heart disease: a delayed autoimmune injury
One cause deserves its own spotlight, because it is so important and so preventable. Rheumatic heart disease follows acute rheumatic fever, which itself follows an untreated group A streptococcal throat infection. Think of strep throat that was never treated. The immune system makes antibodies against the bacteria. But through molecular mimicry, those antibodies also attack the body's own tissues, including the heart valves. Years of smoldering inflammation scar the valve leaflets and fuse them together. The mitral valve is damaged most often, and the classic result is mitral stenosis. This is why treating strep throat with antibiotics truly protects the heart.
Why chronic valve disease drifts toward heart failure
Here is the through-line that ties it all together. The chamber may strain against high pressure (stenosis) or drown in extra volume (regurgitation). Either way it copes for a while by remodeling, thickening or stretching to keep output up. This compensation can last years, and patients often feel fine. But muscle that is overworked for years cannot keep up forever. Thick, stiff walls relax poorly and fill poorly. Stretched, dilated walls squeeze weakly. Either way the ventricle moves less blood forward, pressure backs up into the lungs, and you get the picture of heart failure: dyspnea, fatigue, and fluid congestion. Work out which chamber is overloaded and how. That tells you exactly where the backup and the symptoms will appear. Explore the figure below to see stenosis and regurgitation side by side.
- Two failure modes: stenosis is a stiff, narrowed valve (pressure overload). Regurgitation is a leaky valve that lets blood flow backward (volume overload).
- Signature lesions: aortic stenosis drives concentric hypertrophy of the left ventricle. Mitral regurgitation dilates the left atrium and ventricle (eccentric hypertrophy).
- Rheumatic heart disease comes from untreated group A strep by way of molecular mimicry. It classically scars the mitral valve, so treating strep throat protects the heart.
- The common endpoint: chronic pressure or volume overload is compensated for years. Then the overworked chamber fails, and blood backs up into the lungs as heart failure.
- Watch symptom onset: a compensated patient can feel well for years. New symptoms, especially in aortic stenosis, signal decompensation and need prompt evaluation.
Section 5The EKG & arrhythmias
Your heart has its own built-in electrical wiring, and every heartbeat starts as a tiny spark. Before we talk about what goes wrong, let us walk the normal path that spark travels. Every arrhythmia is really just a detour, a delay, or a short circuit somewhere along that road.
The normal conduction system: the heart's spark and wire
The signal begins in the sinoatrial (SA) node, a patch of cells high in the right atrium. The SA node is the heart's natural pacemaker because it fires fastest, usually 60 to 100 times a minute in an adult at rest. Its spark spreads across both atria and squeezes them. Then it funnels down to the atrioventricular (AV) node. The AV node is the gatekeeper. It holds the signal back a fraction of a second on purpose. That pause lets the atria finish emptying blood into the ventricles before the ventricles contract. From there the current races down the bundle of His and splits into the right and left bundle branches. It fans out through the Purkinje fibers, which fire both ventricles almost at once for a strong, coordinated pump.
Reading the P-QRS-T
An EKG (ECG) is simply a voltage recording of that electrical trip. Each normal beat draws three shapes:
- P wave = atrial depolarization. The atria fire and contract.
- QRS complex = ventricular depolarization. The ventricles fire. It is tall and narrow because the Purkinje system spreads the current so fast.
- T wave = ventricular repolarization. The ventricles reset for the next beat.
To read a strip, check the rate and the rhythm. For rate, count the QRS complexes in a 6-second strip and multiply by 10. You can also use the interval between beats. For rhythm, ask three questions. Is there a P wave before every QRS? Is every QRS narrow? Are the intervals regular? In a normal sinus rhythm the answer is yes to all three. When one of those answers turns to no, you have an arrhythmia (dysrhythmia).
Atrial fibrillation and its stroke risk
In atrial fibrillation (AFib) the atria stop taking their cue from the SA node. Instead they quiver chaotically from many misfiring spots. On the strip the P waves disappear and leave a wavy baseline. The QRS complexes march by irregularly irregular, with no pattern at all. The real danger is not the fast pulse. It is what happens to the blood. The atria only quiver instead of squeezing, so blood pools and sits still, above all in the left atrial appendage. Stagnant blood clots. Recall Virchow's triad, where stasis is one of the three legs. A clot that breaks loose travels to the brain and causes an embolic stroke. That is why patients with AFib are usually placed on anticoagulants.
Heart blocks: a traffic jam at the AV node
A heart block is a delay or a failure of the signal passing from the atria to the ventricles. In first-degree block every beat gets through, just slowly, which shows as a long PR interval. In second-degree block some atrial signals reach the ventricles and some are dropped. In third-degree (complete) block nothing gets through. The atria and ventricles beat on their own and ignore each other. The ventricles fall back on a slow backup pacemaker, often too slow to hold up blood pressure. Complete block frequently needs a pacemaker.
The lethal rhythms
Some arrhythmias are true emergencies. The ventricles are the pumping chambers, and in these rhythms they fail to move blood.
| Rhythm | What the ventricles do | Response |
|---|---|---|
| Ventricular tachycardia (VT) | Fire far too fast from a spot in the ventricle. Wide QRS, little time to fill | Emergency. If there is no pulse, defibrillate and start CPR |
| Ventricular fibrillation (VF) | Only quiver. No organized squeeze, so no cardiac output | Defibrillate right away, plus CPR |
| Asystole | No electrical activity at all. A flatline | CPR plus epinephrine. Not shockable |
VT and VF are shockable because a defibrillator can reset chaotic ventricular activity back into a coordinated rhythm. Asystole is not shockable. There is no electrical activity to reorganize. So the answer is high-quality CPR and drugs, not a shock.
When an arrhythmia is an emergency
The name of the rhythm matters less than how the patient looks. Watch for signs of poor perfusion, which means not enough blood flow to the tissues. Look for chest pain, shortness of breath, low blood pressure, cool clammy skin, confusion, or fainting (syncope). Some rhythms leave the patient with no pulse: VT without a pulse, VF, or asystole. Start CPR and call a code right away. A patient who is awake but unstable still needs urgent treatment. Explore the interactive EKG below to practice spotting P waves and QRS complexes, and the difference between an organized strip and a chaotic one.
- The impulse travels from the SA node to the AV node, which delays it, then to the bundle of His and the Purkinje fibers. The EKG records this as the P wave (atria), the QRS (ventricles firing), and the T wave (ventricles resetting).
- Read a strip by checking rate and rhythm. A P wave before every narrow QRS at a regular interval is normal sinus rhythm.
- Atrial fibrillation is irregularly irregular with no P waves. Quivering atria let blood pool and clot, which raises stroke risk, so patients are usually anticoagulated.
- Heart blocks are delays in AV conduction. Complete (third-degree) block often needs a pacemaker.
- VT, VF, and asystole are lethal. VF and pulseless VT are shockable with defibrillation. Asystole is not, so treat it with CPR and epinephrine.
Section 6Peripheral vascular disease
Your legs are fed by a two-way plumbing system. Arteries carry bright, oxygen-rich blood down from the heart under high pressure to feed the muscles, skin, and nerves. Veins carry the used, oxygen-poor blood back up to the heart against gravity. One-way valves and the squeeze of your calf muscles help push it along. When either half of this system fails, the tissue downstream suffers. It suffers in very different ways, though. It depends on whether the fault is inflow (arterial) or outflow (venous). Peripheral vascular disease is the umbrella term for both.
Arterial disease (PAD): not enough blood getting in
Peripheral arterial disease (PAD) is usually caused by atherosclerosis. It is the same cholesterol plaque that clogs coronary arteries, now narrowing the arteries of the legs. Less blood can squeeze past the plaque, so the muscles are starved of oxygen, above all when they demand more.
The classic early sign is intermittent claudication. It is a cramping, aching pain in the calf, thigh, or buttock. It comes on with walking, in a predictable way, and it reliably eases with rest. The mechanism is simple supply and demand. Exercising muscle needs more oxygen than the narrowed artery can deliver. The muscle switches to anaerobic metabolism, lactic acid builds up, and that causes pain. Rest lowers the demand, the ache resolves, and the cycle repeats at about the same walking distance.
As the disease worsens, the limb shows the hallmark six P's of limb ischemia. There is pain, in time even at rest, and rest pain is often worst at night when the leg is elevated in bed. There is pallor, so the limb turns pale, because little blood is filling the skin. It goes pulseless, or the distal pulses grow faint. Paresthesia is pins and needles from a nerve starved of blood. Paralysis is loss of movement. And poikilothermia means the limb drifts to room temperature, so it feels cool, because warm blood is not arriving. Chronic ischemia leaves the skin shiny, hairless, and thin, with thickened nails, because starved tissue cannot keep up normal growth. Patients often report that dangling the leg over the side of the bed relieves rest pain. Gravity helps pull the meager blood flow downhill.
Venous disease: not enough blood getting out
Chronic venous insufficiency (CVI) is the mirror image. Here the arteries deliver blood fine, but the veins cannot return it. Damaged or incompetent valves let blood flow backward and pool in the legs. That valve damage often follows years of standing, obesity, pregnancy, or a prior clot. Pressure then rises in the veins and capillaries, a state called venous hypertension.
That backed-up pressure pushes fluid out into the tissues. The result is chronic edema that is usually worst by the end of the day and improves overnight. Red blood cells also leak out and break down, leaving iron behind (hemosiderin). The iron stains the skin a permanent brownish color around the lower leg and ankle, a change called stasis dermatitis. Over time the skin becomes leathery and tight (lipodermatosclerosis). The tissue is congested and poorly nourished, so it breaks down into venous ulcers. These classically sit over the inner ankle (the medial malleolus), where venous pressure is highest.
Telling an arterial ulcer from a venous ulcer
Ulcers are where these two get mixed up most often, so match the wound to its mechanism. An arterial ulcer forms because tissue is starved. So it appears where flow is poorest, and it looks dead. A venous ulcer forms because tissue is congested and weepy. So it appears where pooling is worst, and it looks wet.
| Feature | Arterial ulcer | Venous ulcer |
|---|---|---|
| Usual location | Toes, heels, bony points, the lateral (outer) foot | Around the medial (inner) ankle |
| Wound edges | Sharp, punched-out, deep | Uneven, shallow, sloping |
| Wound bed | Pale, gray, or dry. Little drainage | Ruddy, beefy red. Heavy drainage |
| Surrounding skin | Cool, pale, shiny, hairless | Warm, brown-stained, swollen |
| Pain | Severe, and worse when raised | Mild to moderate, better when raised |
| Pulses | Faint or absent | Usually present |
DVT, PE, and one word on aneurysm
A deep vein thrombosis (DVT) is a clot in a deep leg vein. Virchow's triad sets it up: slow venous flow (stasis), injury to the vessel wall, and blood that clots too easily (hypercoagulability). Immobility, surgery, and estrogen are common real-world triggers. The leg is often warm, red, swollen, and tender. The danger is not the leg itself. A piece of clot can break loose, travel to the lungs, and lodge there as a pulmonary embolism (PE). That causes sudden shortness of breath, sharp chest pain with each breath (pleuritic pain), and a drop in oxygen. This is why we never vigorously massage a suspected DVT. Separately, an abdominal aortic aneurysm (AAA) is a balloon-like weak spot in the aortic wall. It may show up as a pulsing (pulsatile) mass in the belly, and it can be fatal if it ruptures. Explore the arterial-versus-venous figure below to see these patterns side by side.
- PAD starves tissue of inflow. You see intermittent claudication, meaning pain with walking that rest relieves, plus a limb that is cool, pale, pulseless, and painful. The pain is worse when the leg is raised.
- Chronic venous insufficiency is an outflow and pooling problem. You see edema, brownish hemosiderin staining, and ulcers around the inner ankle. Raising the leg helps.
- Arterial ulcers are punched-out, dry, and sit on toes and pressure points. Venous ulcers are shallow, wet, and sit around the inner ankle.
- DVT grows out of Virchow's triad. It can throw a clot to the lungs as a pulmonary embolism, which can kill. Do not massage the leg.
- An abdominal aortic aneurysm is a weakened, ballooning aorta that can be fatal if it ruptures.
The chapter in one breath
- Blood pressure is cardiac output times systemic vascular resistance. Hypertension (usually ≥130/80) is the silent disease that is mostly asymptomatic, meaning it causes no symptoms. It thickens vessels and overworks the heart, and it damages the brain, kidneys, and eyes.
- Coronary artery disease is atherosclerotic plaque starving the myocardium. When a plaque ruptures and a clot blocks flow fully, the muscle downstream infarcts. That gives the crushing chest pain, the elevated troponin, and the ST changes of an MI.
- Left-sided heart failure backs blood up into the lungs, so the classic signs are lung signs: crackles, dyspnea, orthopnea, and frothy sputum from pulmonary edema.
- Right-sided heart failure backs blood up into the body, so you see congestion out in the tissues: dependent edema, jugular venous distention, ascites, and a congested, tender liver.
- Valve disorders come in two flavors. Stenosis is a stiff, narrow valve the heart must strain to push through. Regurgitation is a leaky valve that lets blood flow backward. Both force the chamber behind them to thicken or stretch over time.
- The EKG tracks the electrical wave through the heart. The P wave is atrial depolarization, the QRS is ventricular depolarization, and the T wave is ventricular repolarization.
- Atrial fibrillation is the most common serious arrhythmia. It is an irregularly irregular quiver that pools blood in the atria and throws clots. That is why these patients need anticoagulation to prevent stroke.
- Lethal rhythms demand instant action. Ventricular fibrillation and pulseless ventricular tachycardia are shockable, so defibrillate and do CPR. True asystole is not shocked, and is treated with CPR and epinephrine.
- Peripheral vascular disease splits by side. Arterial insufficiency gives pain with walking (claudication), cool pale pulseless feet, and painful wounds far down the limb. Venous insufficiency gives warm swollen legs, brownish skin, and weepy ulcers at the inner ankle.
ReferenceWords worth knowing
A quick reference for the terms in this chapter. Skim it now, or circle back whenever a word trips you up.
- Angina
- Angina is chest pain or pressure that happens when a patch of heart muscle briefly gets less oxygen-rich blood than it needs. The usual reason is a coronary artery narrowed by plaque.
- Atherosclerosis
- Atherosclerosis is the slow buildup of fatty, cholesterol-rich plaque inside artery walls. It stiffens and narrows the vessel, and it can finally block blood flow.
- Atrial fibrillation
- Atrial fibrillation is a fast, disorganized quivering of the atria in place of a coordinated squeeze. Blood pools in the atria, which raises the risk of clots and stroke.
- BNP (B-type natriuretic peptide)
- BNP is a hormone released by stretched, overworked heart muscle. A high blood level often means the heart cannot keep up with its fluid load.
- Cardiac output
- Cardiac output is the amount of blood the heart pumps each minute. It equals heart rate times stroke volume, and in adults it is usually about 4 to 8 L/min.
- Claudication
- Claudication is cramping leg pain that comes on with walking and eases with rest. Narrowed arteries cannot deliver enough blood to working muscle.
- Ejection fraction
- Ejection fraction is the share of blood in a filled ventricle that gets pumped out with each beat, written as a percentage. Normal is about 55 to 70 percent.
- Embolus
- An embolus is a clot, a piece of plaque, an air bubble, or another mass that travels in the bloodstream. It keeps going until it lodges in a smaller vessel and blocks it.
- Heart failure
- Heart failure is the state in which the heart can no longer pump strongly enough, or fill well enough, to meet the body's needs. Fluid backs up and the patient tires easily.
- Hypertension
- Hypertension is blood pressure that stays high, usually 130/80 mmHg or above. It forces the heart to work harder and slowly damages vessel walls and organs.
- Myocardial infarction
- Myocardial infarction, or heart attack, is the death of heart muscle. It happens when a coronary artery is fully blocked and that patch of tissue is starved of oxygen.
- RAAS (renin-angiotensin-aldosterone system)
- RAAS is a hormone cascade that raises blood pressure when blood flow drops. It tightens blood vessels and tells the kidneys to hold on to salt and water.
- Regurgitation
- Regurgitation is blood leaking backward through a heart valve that does not close tightly. The heart must pump extra to make up for what flows the wrong way.
- Stenosis
- Stenosis is abnormal narrowing or stiffening of a heart valve or a vessel. It holds back forward blood flow, so the heart must push harder to move blood through.
- Systemic vascular resistance
- Systemic vascular resistance is the total opposition to blood flow set by the tone of the body's arteries, meaning how tight or relaxed they are. It is a major driver of blood pressure.
- Troponin
- Troponin is a protein released into the blood when heart muscle cells are injured. A rising level is a key marker used to confirm a myocardial infarction.
DrillFlashcards for this unit
These are the Week 9 cards. It is the same deck as the hub, pulled in here so you can review the moment you finish reading. Tap the card to flip it. Hit Shuffle to mix them up. To grade yourself and track mastery across the whole deck, open the full flashcards page.