60 مصطلحاً في مادة نظام القلب والدورة الدموية مع تعريفات مبنية من المنهج المقرّر — كل مصطلح مربوط بدرسه.
The spectrum caused by acute plaque change with thrombus: unstable angina (no necrosis), non-ST-elevation infarction (subendocardial, partial occlusion) and ST-elevation infarction (transmural, complete occlusion).
An abnormal secondary depolarisation during (early, favoured by a long QT) or after (delayed, favoured by calcium overload and digitalis) the action potential; if it reaches threshold it triggers a beat.
The load the ventricle must overcome to eject, set mainly by aortic pressure and vascular resistance; a rise reduces stroke volume unless contractility compensates.
Antineutrophil cytoplasmic antibodies: c-ANCA against proteinase-3, associated with granulomatosis with polyangiitis, and p-ANCA against myeloperoxidase, associated with microscopic polyangiitis and eosinophilic granulomatosis with polyangiitis; they activate neutrophils to damage the vessel wall.
The pathognomonic lesion of rheumatic fever: a focus of fibrinoid necrosis surrounded by lymphocytes, macrophages and Anitschkow cells in the myocardium.
The lesion of atherosclerosis: a raised intimal plaque with a fibrous cap of smooth muscle and collagen over a soft core of lipid, foam cells, necrotic debris and cholesterol clefts.
Chaotic atrial activity at 400 to 600 per minute with no organised P waves, giving an irregularly irregular ventricular response; the atria do not contract, so stroke volume falls and thrombus can form in the appendage.
The ability of a tissue to keep its blood flow nearly constant when arterial pressure changes between about 70 and 175 mmHg, by metabolic and myogenic adjustment of arteriolar tone.
Stretch receptors in the carotid sinus (glossopharyngeal nerve) and aortic arch (vagus) fire faster when pressure rises, inhibiting the vasomotor centre and exciting the vagal centre; it buffers pressure changes within seconds.
Ca2+ entering through L-type channels during the plateau opens ryanodine receptors on the sarcoplasmic reticulum, releasing the much larger store of Ca2+ that drives contraction.
Cardiac output divided by body surface area; about 3 L/min/m² at rest, declining with age.
The volume the left ventricle ejects per minute: heart rate × stroke volume, about 5 L/min in a resting adult, up to 25 L/min in a trained athlete during exercise.
The regulatory proteins troponin I and T of cardiac muscle, released into blood when myocytes die; the most sensitive and specific marker of myocardial infarction.
Coronary arteries behave as functional end arteries: anastomoses exist but are too small to sustain the myocardium when a main branch is suddenly blocked.
Generalised inadequacy of tissue perfusion; hypovolaemic (blood loss, dehydration), cardiogenic (pump failure), obstructive (tamponade, embolism) or distributive (septic, anaphylactic, neurogenic).
Narrowing of the aorta, usually just distal to the left subclavian artery near the ligamentum arteriosum, causing upper-limb hypertension, weak delayed femoral pulses and rib notching from collateral intercostal arteries.
The force of contraction at a given preload and afterload, raised by sympathetic stimulation, catecholamines, calcium and digitalis and lowered by hypoxia, acidosis and beta-blockade.
The large vein in the posterior atrioventricular groove that receives the great, middle and small cardiac veins and opens into the right atrium.
A cardiac glycoside that inhibits the Na+/K+ ATPase, raising intracellular calcium and contractility, and slows atrioventricular conduction through vagal stimulation; narrow therapeutic index.
A calcium channel blocker selective for vascular smooth muscle (amlodipine, nifedipine) that lowers resistance with little direct effect on the heart, unlike verapamil and diltiazem.
The fetal channel from the pulmonary trunk to the aorta, derived from the left sixth aortic arch, that bypasses the lungs; it closes functionally within hours of birth and becomes the ligamentum arteriosum.
A site outside the sinoatrial node that depolarises spontaneously and captures the rhythm, either because its own automaticity is enhanced or because the sinus rate has fallen (escape rhythm).
The equilateral triangle formed by the right arm, left arm and left leg electrodes; leads I, II and III are its sides and lead II = lead I + lead III.
The ventricular volume at the end of filling, about 120 ml in a resting adult; the preload the ventricle contracts against.
An autosomal dominant defect of the LDL receptor (or apoB-100, or a PCSK9 gain of function) causing very high LDL, tendon xanthomas and premature coronary disease; homozygotes have infarcts in childhood.
The long-running community cohort study begun in 1948 in Massachusetts that identified the major cardiovascular risk factors and produced the first multivariable risk scores.
Within physiological limits the heart pumps all the blood that returns to it: a larger end-diastolic volume stretches the sarcomeres toward optimal overlap and raises the force of contraction.
Inability of the heart to pump enough blood to meet metabolic demand, or to do so only at raised filling pressures; classified as systolic (reduced ejection fraction) or diastolic (preserved ejection fraction with impaired filling), and as left, right or biventricular.
The enzyme that converts HMG-CoA to mevalonate, the rate-limiting step of cholesterol synthesis; inhibited by cholesterol, glucagon and statins, activated by insulin.
A genetic disease of sarcomeric proteins producing asymmetric septal hypertrophy, myofibre disarray, diastolic dysfunction and a risk of sudden death in young athletes.
The step-like junction between cardiac muscle cells, containing desmosomes for adhesion and gap junctions for electrical coupling, which makes the myocardium a functional syncytium.
The phase after the atrioventricular valves close and before the semilunar valves open: ventricular pressure rises steeply while volume stays at end-diastolic volume.
Wall tension equals transmural pressure times radius (for a thin-walled sphere, divided by two), so larger vessels and dilated ventricles carry more wall stress.
The cholesterol-rich particle formed from VLDL that delivers cholesterol to tissues through the LDL receptor (apoB-100); the main atherogenic lipoprotein.
The average pressure over the cycle, approximately diastolic pressure plus one third of pulse pressure; the product of cardiac output and total peripheral resistance.
The average direction of ventricular depolarisation in the frontal plane; normal from -30 to +90 degrees.
The central compartment of the thorax between the two pleural sacs, divided into superior and inferior parts; the inferior part has anterior, middle (heart and pericardium) and posterior divisions.
The balance of the Starling forces: (capillary hydrostatic − interstitial hydrostatic) − (plasma oncotic − interstitial oncotic); slightly positive on average, so lymph carries the excess.
Atrial depolarisation spreading from the sinoatrial node; normally upright in lead II and under 0.12 s.
The fibrous sac around the heart lined by serous pericardium (parietal and visceral layers); the pericardial cavity between the serous layers holds a thin film of fluid.
The prolonged depolarised phase of the ventricular action potential, maintained by inward L-type Ca2+ current balanced against outward K+ current; it lengthens the refractory period.
Flow through a tube is proportional to the pressure gradient and the fourth power of the radius, and inversely proportional to length and viscosity; halving the radius cuts flow sixteenfold.
Shifting the whole distribution of a risk factor by a small amount through policy and environment, which prevents more disease in total than treating only the high-risk tail, as shown by the North Karelia programme.
Sites where portal and systemic veins communicate (oesophageal, rectal, para-umbilical, retroperitoneal); they enlarge in portal hypertension.
From the start of the P wave to the start of the QRS: atrial depolarisation plus the delay in the atrioventricular node; 0.12 to 0.20 s.
The stretch of the ventricular fibres at the end of diastole, set by venous return and estimated clinically from end-diastolic volume or pressure.
The rise in renal salt and water excretion when arterial pressure rises; because it has infinite gain over time, the kidney sets the long-term level of arterial pressure.
Ventricular depolarisation, septum first then the free walls; under 0.12 s when conduction through the bundle branches is normal.
A self-sustaining circuit in which an impulse returns to re-excite tissue it has already passed through; it requires two pathways, unidirectional block in one and conduction slow enough for the tissue ahead to recover excitability.
Renin from the juxtaglomerular cells converts angiotensinogen to angiotensin I; angiotensin-converting enzyme forms angiotensin II, a vasoconstrictor that also stimulates aldosterone, sodium retention and thirst.
A dimensionless index (velocity × diameter × density ÷ viscosity) above about 2000 flow becomes turbulent; high velocity, large diameter and low viscosity (anaemia) favour turbulence.
The sound of aortic and pulmonary valve closure at the start of diastole; the pulmonary component normally follows the aortic one and the gap widens on inspiration.
From the end of the QRS to the start of the T wave, when the whole ventricle is depolarised; normally on the baseline, so elevation or depression signals injury or ischaemia.
End-diastolic volume minus end-systolic volume, about 70 ml at rest; ejection fraction is stroke volume divided by end-diastolic volume, normally 55 to 70 percent.
A drug that lowers pressure by reducing sympathetic outflow or blocking its receptors: central alpha-2 agonists, alpha-1 blockers, beta-blockers.
No atrial impulse reaches the ventricles; P waves and QRS complexes march independently and a junctional or ventricular escape rhythm at 20 to 40 per minute sustains the circulation.
A polymorphic ventricular tachycardia with a twisting axis that arises on a prolonged QT interval, provoked by class Ia and III drugs, hypokalaemia and hypomagnesaemia; treated with magnesium.
The resistance of the whole systemic circulation, mean arterial pressure minus right atrial pressure divided by cardiac output; about 1 peripheral resistance unit (mmHg·min/ml) at rest.
Dilated, tortuous superficial veins of the leg produced by sustained raised venous pressure and incompetent valves; complicated by stasis dermatitis, ulceration and superficial thrombophlebitis.
A mass of fibrin, platelets and, in infective endocarditis, microorganisms attached to a valve; large, friable and destructive in infection, small and sterile in marantic and Libman–Sacks endocarditis.