Lecture 6 Cardiac and Lecture 7 Vascular, condensed. Lectures 8–10 are added as each is posted. Mechanism only, never management.
| Term | What you need to know |
|---|---|
| Coronary heart disease | Insufficient delivery of oxygenated blood to the myocardium because of ATHEROSCLEROTIC coronary arteries. About 50% of cardiovascular deaths. Also called ischemic heart disease, coronary artery disease. |
| Ischemia = supply vs demand | Begins when oxygen SUPPLY < DEMAND → less ATP (adenosine triphosphate). Causes abnormal function AND abnormal rhythms; prolonged → irreversible damage. |
| Supply falls | Large plaques · acute platelet aggregation then thrombosis · VASOSPASM · abnormal microcirculation · poor perfusion pressure. |
| Demand rises | Workload = HEART RATE · PRELOAD · AFTERLOAD · CONTRACTILITY. Raise any one → more oxygen demand. |
| Etiologies | ATHEROSCLEROSIS behind almost all → predisposes to thrombosis, vasospasm, endothelial dysfunction. Microcirculation: small-vessel endothelium regulates flow abnormally. Uncommon: low blood oxygen content (respiratory); poor perfusion (hypotension, hypovolemia). |
| Major risk factors | Age · family history · abnormal lipids · smoking · hypertension · diabetes mellitus · obesity. |
| Probable risk factors | Male sex · HOMOCYSTEINE · high-sensitivity C-reactive protein. |
| Collateral circulation | Develops when plaque builds over YEARS — why slow occlusion is tolerated better than sudden. |
| Flow tracks demand | Myocardial oxygen consumption and blood flow correspond NEARLY LINEARLY; METABOLIC SIGNALS are the principal determinants of delivery. |
| Coronary anatomy | LEFT MAIN → left anterior descending (anterior interventricular) + CIRCUMFLEX. RIGHT CORONARY → marginal + posterior interventricular. |
| Frank–Starling | More diastolic filling → more ejected. Force ∝ initial sarcomere length (preload). Maximal force at 2.6 micrometers, rarely exceeded in the normal heart. |
| Term | What you need to know |
|---|---|
| Low-density lipoprotein | Cholesterol-rich → HIGHEST risk. |
| Very-low-density lipoprotein | Triglyceride-rich → INCREASES risk. |
| High-density lipoprotein | DECREASES risk — carries cholesterol BACK TO THE LIVER, away from plaque. |
| Familial hypercholesterolemia | Most common genetic hyperlipidemia. Defective LOW-DENSITY LIPOPROTEIN RECEPTOR on liver cells → liver cannot clear cholesterol. |
| Homocysteine | Amino acid from METHIONINE → CYSTEINE. Atherogenic + prothrombotic: intimal thickening, elastic lamina disruption, smooth muscle hypertrophy, platelet accumulation, platelet-rich occlusive thrombus. |
| Plaque sequence | ENDOTHELIAL INJURY (wall stress, toxins, inflammation, hyperlipidemia) → permeable endothelium, leukocytes recruited → low-density lipoprotein leaks in and is OXIDIZED → FOAM CELLS → mediators + growth factor → smooth muscle proliferation → LIPID CORE → collagen/fibrin CAP. |
| 75% | Occlusion at which blood flow is COMPROMISED. |
| Vulnerable plaque (slide 24, image only) | LARGE lipid core · THIN fibrous cap · rich in MACROPHAGES · increased MMPs (matrix metalloproteinases) · POOR in smooth muscle · LOW-GRADE stenosis. |
| Stable vs vulnerable | Stable: thick cap, small core, many smooth muscle cells. Vulnerable: thin cap, large core, many macrophages. Smooth muscle BUILDS the cap; macrophages DIGEST it. |
| Why plaques rupture | Composition + mechanical stress. Trigger: SHEAR from high-velocity flow through a severe stenosis. VASA VASORUM capillaries hemorrhage → pressure builds inside the plaque. |
| Rupture consequences | Exposed subendothelial proteins → platelet aggregation → THROMBUS; EMBOLI block smaller vessels downstream. |
| Term | What you need to know |
|---|---|
| Coronary syndromes | CHRONIC: stable angina, ischemic cardiomyopathy. ACUTE: unstable angina, myocardial infarction. Classified by severity and onset. |
| Angina pectoris | Intermittent ischemia NOT enough to kill cells; when demand rises; may cause pulmonary congestion. |
| Stable (typical) | MOST COMMON. Fixed stenosis → ischemia only under increased WORKLOAD. |
| Prinzmetal (variant) | VASOSPASM (cause unknown). Unpredictable; NO relation to physical or emotional stress. |
| Unstable (crescendo) | May progress to acute ischemia → counted with the ACUTE coronary syndromes. |
| Acute coronary syndrome | Unstable angina + myocardial infarction (hard to tell apart clinically). Pain longer than typical angina; PLAQUE RUPTURE + ACUTE THROMBOSIS. |
| Infarction mechanism | Prolonged/total loss of flow → NECROSIS or APOPTOSIS. Thrombus on a cracked plaque → platelet plug → clotting cascade → occlusion. Outcome depends on COLLATERALS, WORKLOAD, TIME. |
| Occlusion timeline | Immediately: ATP depleted. Few minutes: cannot contract. AFTER 30 MINUTES: irreversible necrosis. |
| Location | Nearly all in LEFT VENTRICLE. Left anterior descending 40–50% · right coronary 30–40% · left circumflex 15–20%. |
| Gross changes | 6 h: first visible · 18–24 h: paler · then yellow, soft, red vascular border · 1–2 weeks: necrotic tissue removed · by 6 weeks: fibrous scar. |
| Term | What you need to know |
|---|---|
| Stenosis vs regurgitation | STENOSIS = fails to OPEN → PRESSURE work, gradient across valve. REGURGITATION = fails to CLOSE → VOLUME work. |
| Stenosis facts | Hemodynamics affected at 50% closure; slow → compensatory HYPERTROPHY. Causes: RHEUMATIC scarring, aging CALCIFICATION. |
| Regurgitation facts | Acute: infection or PAPILLARY MUSCLE RUPTURE. Causes: rheumatic heart disease, infective endocarditis. |
| Mitral stenosis | DIASTOLIC left atrial > left ventricular gradient. Left atrial congestion/pressure ↑, pulmonary pressure ↑, stroke volume ↓ → pulmonary hypertension → right heart failure. Late: ATRIAL FIBRILLATION, atrial enlargement, ATRIAL CLOTS. |
| Mitral regurgitation | SYSTOLIC backflow into atrium. HIGH AFTERLOAD INCREASES it. Atrium AND ventricle dilate + hypertrophy; severe → left heart failure. |
| Mitral valve prolapse | BALLOONING into left atrium in systole. Usually silent; sometimes some regurgitation. |
| Aortic stenosis | Most often AGE-RELATED CALCIFICATION; common with BICUSPID valve (slide: clinically apparent over 79). Systolic left ventricle–aortic gradient → LEFT VENTRICULAR HYPERTROPHY → ischemia and ANGINA → failure. |
| Aortic regurgitation | DIASTOLIC leak back into left ventricle. AORTIC ROOT DILATION common (aging, connective tissue disease). Left ventricle hypertrophies + dilates; DIASTOLIC PRESSURE FALLS. |
| Timing rule | DIASTOLE: mitral stenosis, aortic regurgitation. SYSTOLE: mitral regurgitation, prolapse, aortic stenosis. |
| Term | What you need to know |
|---|---|
| Rheumatic heart disease | After GROUP A BETA-HEMOLYTIC STREPTOCOCCUS. IMMUNE attack by CROSS-REACTIVITY; HLA (human leukocyte antigen) predisposition. All layers → carditis. Valves: swelling, erosions, platelets + fibrin, then SCARRING and SHORTENING. |
| Infective endocarditis | Invasion + colonization of endocardium; BLOODSTREAM INVASION is a prerequisite. VEGETATIONS = organisms in FIBRIN → dysfunction + EMBOLI. Commonest: Streptococcus, Staphylococcus aureus. |
| Subacute endocarditis | Insidious; needs a PREEXISTING valve lesion. LESS VIRULENT organisms (typically Streptococcus) cannot attack a healthy endocardium. S. aureus is ACUTE, not subacute (the slide lists it here; Robbins pairs it with the acute form). |
| Myocarditis | Inflammation + leukocyte infiltration + necrosis. Microbes, immune disease, physical agents; COXSACKIEVIRUS most common in North America. Left ventricular dysfunction, ALL FOUR chambers dilated, edematous muscle, endocardium usually NORMAL. |
| Dilated cardiomyopathy | Also 'congested'. Dilation of one or both ventricles → failure. ALCOHOL · GENETICS · PREGNANCY · POST-VIRAL. |
| Hypertrophic cardiomyopathy | Thick, HYPERKINETIC muscle. OUTFLOW OBSTRUCTION + impaired DIASTOLIC FILLING. |
| Restrictive cardiomyopathy | Stiff, FIBROTIC, noncompliant (e.g. AMYLOIDOSIS) → restricted filling → low stroke volume → failure. |
| Pericardial effusion types | SEROUS transudate (heart failure, hypoproteinemia) · SEROSANGUINOUS (blunt trauma, heart surgery, cardiopulmonary resuscitation) · CHYLOUS (lymph obstruction) · BLOOD/hemopericardium (penetrating trauma). |
| Tamponade | Large effusion COMPRESSES chambers from outside → filling impaired. Life-threatening. |
| Pericarditis | ACUTE: mostly idiopathic, mostly VIRAL. CHRONIC: ADHESIVE mediastinopericarditis (heart stuck to mediastinum → workload ↑) or CONSTRICTIVE (dense scarred sac = STIFF CAGE → impaired diastolic filling). |
| Not in the deck | Objective m (blood pressure regulation) → see Lecture 7. Objective n (conduction system): no slide; only ischemia → abnormal rhythms, mitral stenosis → atrial fibrillation. |
| Term | What you need to know |
|---|---|
| Five components | ARTERIES high pressure, strong walls, fast flow → ARTERIOLES control release into capillaries (main resistance, 'small but mighty') → CAPILLARIES exchange → VENULES collect → VEINS return blood, RESERVOIR, low pressure, thin walls. |
| Three layers | INTIMA: endothelium on basement membrane + thin matrix. MEDIA: elastin + smooth muscle 'like tree rings', expand in systole, recoil in diastole. ADVENTITIA: loose connective tissue, nerves, its own small arterioles in large vessels. |
| Capillaries | NO MEDIA. ≈ red cell diameter. Large cross-section, LOW flow → easy exchange. Densest in MYOCARDIUM and BRAIN. Pericytes around them. |
| Capillary types | CONTINUOUS (least permeable; blood–brain barrier) · FENESTRATED (kidney glomeruli, small intestine) · SINUSOIDAL (leakiest; liver, marrow, spleen, endocrine). |
| Functions | Nutrients in · wastes out · hormones carried · HOMEOSTASIS of tissue fluid. |
| Loops | PULMONARY: right heart → lungs. SYSTEMIC: left heart → tissues → right heart. Artery = AWAY from heart, so pulmonary artery carries deoxygenated blood. |
| Veins hold | About 66% of total blood volume. |
| Term | What you need to know |
|---|---|
| Healthy endothelium | NONTHROMBOGENIC; modulates medial tone (resistance); METABOLIZES ANGIOTENSIN; regulates inflammation; controls smooth muscle growth. |
| Smooth muscle cells | Predominant media cell. Proliferate; make collagen, elastin, proteoglycans, growth factors, cytokines; constrict/dilate. |
| Neointimal hyperplasia | Injury → smooth muscle MIGRATES INTO INTIMA, proliferates, makes matrix; endothelium regrows with LESS NITRIC OXIDE; platelets activate; leukocytes recruited → thick intima, NARROW LUMEN. Same response to ANY injury. |
| The twofold problem | Thicker intima narrows the lumen AND lost nitric oxide (a vasodilator) lets it constrict. |
| Two mechanisms | NARROWING (progressive: atherosclerosis; precipitous: thrombosis, embolism) or WEAKENING (dilation, rupture). |
| Size predicts disease | LARGE elastic (aorta 2–3.5 cm) → ANEURYSM (elastic loss). MEDIUM muscular (coronary 3–4 mm, renal) → ATHEROSCLEROSIS. SMALL (≤2 mm) + ARTERIOLES (20–100 micrometers) → HYPERTENSION. |
| Blood pressure | = CARDIAC OUTPUT × VASCULAR RESISTANCE. Resistance set at ARTERIOLES (constrictors vs dilators). Output = rate × stroke volume; volume set by SODIUM (water follows sodium). |
| Low pressure response | Kidney RENIN (low afferent arteriolar pressure) → angiotensinogen → ANGIOTENSIN I → endothelial catabolism → ANGIOTENSIN II → smooth muscle tone ↑ + ALDOSTERONE ↑ (sodium resorption). |
| Hypertension risks | Atherosclerosis, congestive heart failure, renal failure, CEREBRAL HEMORRHAGE, AORTIC DISSECTION. |
| Essential hypertension | 90–95%, idiopathic. Genetic + environmental. INSUFFICIENT RENAL SODIUM EXCRETION → volume ↑ → output ↑ → constriction → pressure ↑. |
| Secondary hypertension | RENOVASCULAR: renal artery stenosis → low afferent pressure → RENIN. PRIMARY HYPERALDOSTERONISM: a common cause. |
| Term | What you need to know |
|---|---|
| Arteriosclerosis | 'Hardening of the arteries': wall thickening + LOSS OF ELASTICITY. Four patterns below. |
| Arteriolosclerosis | Small arteries/arterioles; HYPERTENSION. HYALINE = protein-thickened glassy wall, narrow lumen. HYPERPLASTIC = ONION SKINNING (concentric smooth muscle). |
| Fibromuscular intimal hyperplasia | Muscular arteries; inflammation or mechanical injury; a healing response → IN-STENT RESTENOSIS; limits solid-organ transplants. |
| Mönckeberg medial sclerosis | CALCIFICATION OF THE MEDIA of muscular arteries; usually NOT clinically significant. |
| Atherosclerosis | 'Gruel' + 'hardening'. MOST clinically relevant. Coronary, cerebral, peripheral disease; about half of Western deaths. |
| Risk factors | Hyperlipidemia · LIPOPROTEIN(a) (altered low-density lipoprotein, independent of total cholesterol) · smoking · hypertension · diabetes · METABOLIC SYNDROME · C-reactive protein · FAMILY HISTORY = MOST IMPORTANT · age · men + postmenopausal women. |
| Sequence | Injury → LOW-DENSITY LIPOPROTEIN accumulates → MONOCYTE adhesion → PLATELET adhesion → smooth muscle RECRUITED → proliferation, matrix, T cells → lipid → CALCIFICATION. |
| Atheroma | Intimal plaque into the lumen: SOFT LIPID CORE + FIBROUS CAP. Stable → ischemia; unstable → rupture, thrombosis, embolism. |
| ★ Peripheral arterial disease | 'Do know': stenosis → ischemia → CLAUDICATION when working muscle's demand rises. |
| Term | What you need to know |
|---|---|
| Aneurysm vs dissection | ANEURYSM = localized abnormal DILATION. DISSECTION = blood enters a wall defect and TUNNELS through the MEDIA. |
| Shapes | TRUE saccular (focal bulge, 'berry') · TRUE fusiform (whole circumference) · FALSE (ruptured wall, hematoma held by extravascular tissue) · DISSECTION (intimal tear splits media). |
| Weakening ≠ rupture | An aneurysm is a WEAK wall, not a ruptured one; rupture risk rises with SIZE (in lecture: under 4 cm rarely, over 5.5 cm very high). |
| Pathogenesis | Poor connective tissue (defective collagen; abnormal transforming growth factor signaling = MARFAN) · collagen degradation > synthesis (inflammation, proteases) · smooth muscle LOSS (ischemia, hypertension, TERTIARY SYPHILIS). |
| Predisposing | Atherosclerosis · hypertension · smoking. |
| Abdominal aortic aneurysm | ATHEROSCLEROTIC; abdominal aorta + common iliac arteries. |
| Thoracic aortic aneurysm | HYPERTENSION; also Marfan, inflammation. |
| Aortic dissection | Laminar planes of MEDIA SPLIT → blood channel in the wall. HYPERTENSION = major risk factor. |
| Cerebral saccular (berry) | Thin/absent media; absent or fragmented internal elastic lamina. LACK OF ELASTIC LAMINA = main feature. Usually acquired. |
| Fusiform / mycotic | Fusiform: whole circumference (atherosclerosis). MYCOTIC: infected emboli from INFECTIVE ENDOCARDITIS (rare). |
| Term | What you need to know |
|---|---|
| Fibromuscular dysplasia | Focal irregular thickening (hyperplasia + fibrosis of MEDIA and INTIMA) of medium/large muscular arteries → stenosis. RENAL arteries. 'STRING OF BEADS' on angiography; may dilate and rupture. |
| Vasculitis | Vessel wall inflammation, mostly SMALL vessels. Mechanisms: IMMUNE-MEDIATED or DIRECT INFECTIOUS INVASION. Large: giant cell arteritis. Medium: polyarteritis nodosa, Kawasaki. Small: ANCA (anti-neutrophil cytoplasmic antibody) necrotizing; immune complex (lupus, rheumatoid arthritis). Said to go light. |
| Raynaud phenomenon | EXAGGERATED VASOCONSTRICTION to COLD + STRESS, extremities. WHITE (spasm) → BLUE (anoxia) → RED (oxygenated blood returns). |
| Arteriovenous fistula | Direct artery–vein link BYPASSING CAPILLARIES: developmental, aneurysm rupturing into a vein, penetrating injury, inflammatory necrosis, surgical (hemodialysis access). |
| Veins | Larger lumen, THINNER MEDIA (capacitance), VALVES stop gravitational backflow. |
| Varicose veins | Dilated, tortuous; VALVE INSUFFICIENCY; chronic high intraluminal pressure + weak wall. Superficial (saphenous), legs; also pelvis/rectum. |
| Esophageal varices / hemorrhoids | Varices: submucosal distal esophageal veins from CIRRHOSIS + PORTAL HYPERTENSION. Hemorrhoids: varicose venous plexus at the ANORECTAL junction. |
| Deep vein thrombosis | Deep veins (femoral, popliteal, tibial); STASIS in a dilated vein. THIRD most common cardiovascular cause of death. |
| Deep vein thrombosis risks | Reduced flow (IMMOBILITY) · raised venous pressure · mechanical injury · raised viscosity (dehydration, thrombocytosis) · anatomy · hypercoagulable (cancer, sepsis, lupus, ORAL ESTROGEN). |
| Virchow triad | VESSEL WALL DAMAGE · FLOW TURBULENCE · HYPERCOAGULABILITY. |
| Clot fate | Neutrophils + macrophages infiltrate fibrin; COLLAGEN replaces fibrin over weeks → less flow. Dislodges → EMBOLUS → PULMONARY ARTERY = pulmonary embolus. |