Heart Flashcards
(121 cards)
1
Q
The Systemic Circulation
A
The Systemic Circulation
- Blood flows from the left ventricle into the aorta and from the aorta into arteries that eventually branch into arterioles and capillaries, the smallest of the arterial vessels. Oxygen, nutrients, and other substances needed for cellular metabolism pass from the capillaries into the interstitium, where they are taken up by the cells. Capillaries also absorb metabolic waste products from the interstitium.
The Lymphatic System
- The vessels of the lymphatic system run in the same sheaths as the arteries and veins.
- Lymph (interstitial fluid) is absorbed by lymphatic venules in the capillary beds and travels
through ever larger lymphatic veins until it empties through the right lymphatic duct or thoracic
duct into the right or left subclavian veins, respectively. - As lymph travels toward the thoracic ducts, it passes through thousands of lymph nodes clustered
around the lymphatic veins. The lymph nodes are sites of immune function and are ideally placed to sample antigens and cells carried by the lymph from the periphery of the body into the central circulation.
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Q
Overview
A
- The circulatory system is part of the body’s transport and communication systems. It delivers oxygen, nutrients, metabolites, hormones, neurochemicals, proteins, and blood cells including lymphocytes and leukocytes throughout the body and carries metabolic wastes to the kidneys, lungs, and liver for excretion.
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Q
The Circulatory System
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- The circulatory system consists of the heart and the blood and lymphatic vessels and is made up of two separate, but conjoined serially connected pump systems: the pulmonary circulation and the systemic circulation. The lymphatic system is a one-way network consisting of lymphatic vessels and lymph nodes.
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Q
The Circulatory System
A
- The low-pressure pulmonary circulation is driven by the right side of the heart; its function is to deliver blood to the lungs for oxygenation.
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Q
The Circulatory System
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- The higher pressure systemic circulation is driven by the left side of the heart and functions to provide oxygenated blood, nutrients, and other key substances to body tissues and transport waste products to the lungs, kidneys, and liver for excretion
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Q
The Circulatory System
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4. The lymphatic vessels collect fluids from the interstitium and return the fluids to the circulatory system; lymphatic vessels also deliver antigens, microorganisms, and cells to the lymph nodes.
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Q
The heart
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- The heart consists of four chambers (two atria and two ventricles), four valves (two atrioventricular valves [AV valves] and two semilunar valves), a muscular wall, a fibrous skeleton, a conduction system, nerve fibres, systemic vessels (the coronary circulation), and openings where the great vessels enter the atria and ventricles.
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Q
heart
A
- The heart wall, which encloses the heart and divides it into chambers, is made up of three layers: the epicardium (outer layer), the myocardium (muscular layer), and the endocardium (inner lining). The heart lies within the pericardium, a double-walled membranous sac.
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Q
heart
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- The myocardial layer of the two atria, which receive blood entering the heart, is thinner than the myocardial layer of the ventricles, which have to be stronger to squeeze blood out of the heart.
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Q
heart
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- The right and left sides of the heart are separated by portions of the heart wall called the interatrial septum and the interventricular septum.
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heart
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- Deoxygenated (venous) blood from the systemic circulation enters the right atrium through the superior and inferior venae cavae. From the right atrium, the blood passes through the right AV (tricuspid) valve into the right ventricle. In the ventricle, the blood flows from the inflow tract to the outflow tract and then through the pulmonary semilunar valve (pulmonary valve) into the pulmonary artery, which delivers it to the lungs for oxygenation.
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Q
heart
A
- Oxygenated blood from the lungs enters the left atrium through the four pulmonary veins (two from the left lung and two from the right lung). From the left atrium, the blood passes through the left AV valve (mitral valve) into the left ventricle. In the ventricle, the blood flows from the inflow tract to the outflow tract and then through the aortic semilunar valve (aortic valve) into the aorta, which delivers it to systemic arteries of the entire body.
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Q
heart
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- There are four heart valves. The AV valves ensure one-way flow of blood from the atria to the ventricles. The semilunar valves ensure one-way blood flow from the right ventricle to the pulmonary artery and from the left ventricle to the aorta.
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Q
heart
A
- Oxygenated blood enters the coronary arteries through openings from the aorta, and
deoxygenated blood from the coronary veins enters the right atrium through the coronary sinus.
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Q
heart
A
- The pumping action of the heart consists of two phases: diastole, during which the myocardium
relaxes and the ventricles fill with blood; and systole, during which the myocardium contracts, forcing blood out of the ventricles. A cardiac cycle includes one systolic contraction and the diastolic relaxation that follows it. Each cardiac cycle represents one heartbeat.
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Q
heart
A
- The conduction system of the heart generates and transmits electrical impulses (cardiac action potentials) that stimulate systolic contractions. The autonomic nerves (sympathetic and parasympathetic fibres) can adjust heart rate and force of contraction, but they do not originate the heartbeat.
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Q
heart
A
- Each cardiac action potential travels from the SA node to the AV node to the bundle of His (atrioventricular bundle [AV bundle]), through the bundle branches, and finally to the Purkinje fibres and ventricular myocardium, where the impulse stops. It is prevented from reversing its path by the refractory period of cells that have just been polarized. The refractory period ensures that diastole (relaxation) will occur, thereby completing the cardiac cycle.
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Q
heart
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- The normal electrocardiogram is the sum of all cardiac action potentials. The P wave represents atrial depolarization; the QRS complex is the sum of all ventricular cell depolarizations. The ST interval occurs when the entire ventricular myocardium is depolarized.
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Q
heart
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- Cells of the cardiac conduction system possess the properties of automaticity and rhythmicity. Automatic cells return to threshold and depolarize rhythmically without an outside stimulus. The cells of the SA node depolarize faster than other automatic cells, making it the natural pacemaker of the heart. If the SA node is disabled, the next fastest pacemaker, the atrioventricular node (AV node), takes over.
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heart
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- Cardiac action potentials are generated by the sinoatrial node (SA node) at a rate of 60 to 100 impulses per minute. The impulses can travel through the conduction system of the heart, stimulating myocardial contraction as they go.
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heart
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- Adrenergic receptor number, type, and function govern autonomic (sympathetic) regulation of heart rate, contractile strength, and the dilation or constriction of coronary arteries. The presence of specific receptors on the myocardium and coronary vessels determines the effects of the neurotransmitters norepinephrine and epinephrine.
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heart
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- Unique features that distinguish myocardial cells from skeletal cells enable myocardial cells to transmit action potentials faster (through intercalated discs), synthesize more adenosine triphosphate (because of a large number of mitochondria), and have readier access to ions in the interstitium (because of an abundance of transverse tubules). These combined differences enable the myocardium to work constantly, which is not required by skeletal muscle.
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heart
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- Cross-bridges between actin and myosin enable contraction. Calcium ions interacting with the troponin complex help initiate the contraction process. Subsequently, myocardial relaxation begins as troponin releases calcium ions.
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Q
heart
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- Cardiac performance is affected by preload, afterload, myocardial contractility, and heart rate.
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heart
19. Preload, or pressure generated in the ventricles at the end of diastole, depends on the amount of
blood in the ventricle. Afterload is the resistance to ejection of the blood from the ventricle.
Afterload depends on pressure in the aorta.
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heart
20. Myocardial stretch determines the force of myocardial contraction; thus the greater the stretch, the
stronger the contraction up to a certain point. This relationship is known as Starling's law of the
heart.
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heart
21. Contractility is the potential for myocardial fibre shortening during systole. It is determined by
the amount of stretch during diastole (i.e., preload) and by sympathetic stimulation of the
ventricles.
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heart
22. Heart rate is determined by the SA node and by components of the autonomic nervous system,
including cardiovascular control centres in the brain, receptors in the aorta and carotid arteries, and hormones, including catecholamines (epinephrine, norepinephrine).
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systemic circulation
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15. Venous blood pressure is influenced by blood volume within the venous system and compliance of the venous walls.
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systemic circulation
2. Venules, the smallest veins, receive capillary blood. From the venules, the venous blood flows into larger and larger veins until it reaches the venae cavae, through which it enters the right atrium.
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systemic circulation
3. Blood vessel walls have three layers: (1) the tunica intima (inner layer), (2) the tunica media (middle layer), and (3) the tunica externa (the outer layer)
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systemic circulation
4. Layers of the blood vessel wall differ in thickness and composition from vessel to vessel, depending on the vessel's size and location within the circulatory system. In general, the tunica media of arteries close to the heart has more elastic fibres because these arteries must be able to distend during systole and recoil during diastole. Distributing arteries farther from the heart contain more smooth muscle fibres because they constrict and dilate to control blood pressure and volume within specific capillary beds.
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systemic circulation
5. Blood flow into the capillary beds is controlled by the contraction and relaxation of smooth muscle bands (precapillary sphincters) at junctions between metarterioles and capillaries.
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systemic circulation
6. Endothelial cells line the blood vessels. The endothelium is a life-support tissue; it functions as a filter (altering permeability), changes in vasomotion (constriction and dilation), and is involved in clotting and inflammation.
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systemic circulation
7. Blood flow through the veins is assisted by the contraction of skeletal muscles (the muscle pump), and backward flow is prevented by one-way valves, which are particularly important in the deep veins of the legs.
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systemic circulation
8. Blood flow is affected by blood pressure, resistance to flow within the vessels, blood consistency (which affects velocity), anatomical features that may cause turbulent or laminar flow, and compliance (distensibility) of the vessels.
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systemic circulation
9. Poiseuille's law describes the relationship of blood flow, pressure, and resistance as the difference between pressure at the inflow end of the vessel and pressure at the outflow end divided by resistance within the vessel.
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systemic circulation
10. The greater a vessel's length and the blood's viscosity and the narrower the radius of the vessel's lumen, the greater the resistance within the vessel.
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systemic circulation
11. Total peripheral resistance, or the resistance to flow within the entire systemic circulatory system, depends on the combined lengths and radii of all the vessels within the system and on whether the vessels are arranged in series (greater resistance) or in parallel (lesser resistance).
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systemic circulation
12. Blood flow is also influenced by neural stimulation (vasoconstriction or vasodilation) and by autonomic features that cause turbulence within the vascular lumen (e.g., protrusions from the vessel wall, twists and turns, vessel branching).
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systemic circulation
13. Arterial blood pressure is influenced and regulated by factors that affect cardiac output (heart rate, stroke volume), total resistance within the system, and blood volume.
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systemic circulation
14. Antidiuretic hormone, the renin-angiotensin-aldosterone system, and natriuretic peptides can all alter blood volume and thus blood pressure.
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systemic circulation
16. Blood flow through the coronary circulation is governed by the same principles as flow through other vascular beds plus two adaptations dictated by cardiac dynamics. First, blood flows into the coronary arteries during diastole rather than systole, because during systole the cusps of the aortic semilunar valve block the openings of the coronary arteries. Second, systolic contraction inhibits coronary artery flow by compressing the coronary arteries.
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systemic circulation
18. Autoregulation enables the coronary vessels to maintain optimal perfusion pressure despite
systolic compression.
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systemic circulation
17. Myoglobin in heart muscle stores oxygen for use during the systolic phase of the cardiac cycle.
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venous disorders
Varicosities are areas of veins in which blood has pooled, usually in the saphenous veins. Varicosities may be caused by damaged valves as a result of trauma to the valve or by chronic venous distension involving gravity and venous constriction.
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venous disorders
2. Chronic venous insufficiency (CVI) is inadequate venous return over a long period that causes pathological ischemic changes in the vasculature, skin, and supporting tissues.
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venous disorders
3. Venous stasis ulcers follow the development of CVI and probably develop as a result of the borderline metabolic state of the cells in the affected extremities.
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venous disorders
4. Deep venous thrombosis (DVT) results from stasis of blood flow, endothelial damage, or hypercoagulability. The most serious complication of DVT is pulmonary embolism.
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venous disorders
5. Superior vena cava syndrome is a progressive occlusion of the superior vena cava that leads to venous distension in the upper extremities and head. Because this syndrome is usually caused by bronchogenic cancer, it is generally considered an oncological emergency rather than a vascular emergency.
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1
1. Hypertension is the elevation of systemic arterial blood pressure resulting from increases in cardiac output (blood volume), total peripheral resistance, or both.
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disorders of arteries
2. Hypertension can be primary (without a known cause) or secondary (caused by an underlying disease).
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disorders of arteries
3. The risk factors for hypertension include family history; gender (men greater than women before age 55; women greater than men after 55); advancing age; being of African descent; being of Indigenous descent; recent immigration; obesity; high dietary sodium intake; dietary intake of potassium, calcium, and magnesium; glucose intolerance; cigarette smoking; and heavy alcohol consumption.
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disorders of arteries
4. The exact cause of primary hypertension is unknown, although several hypotheses are proposed, including overactivity of the sympathetic nervous system (SNS); overactivity of the renin- angiotensin-aldosterone system (RAAS); sodium and water retention by the kidneys; hormonal inhibition of sodium–potassium transport across cell walls; and complex interactions involving insulin resistance, inflammation, and endothelial function.
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disorders of arteries
5. Clinical manifestations of hypertension result from damage of organs and tissues outside the vascular system. These include retinal changes, heart disease, renal disease, and central nervous system disorders, such as stroke and dementia.
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disorders of arteries.
Hypertension is managed with both pharmacological and nonpharmacological methods that lower the blood volume and the total peripheral resistance.
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disorders of arteries
7. Orthostatic hypotension (OH) is a drop in blood pressure that occurs on standing. The compensatory vasoconstriction response to standing is replaced by a marked vasodilation and blood pooling in the muscle vasculature.
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disorders of arteries
10. A thrombus is a clot that remains attached to a vascular wall. An embolus is a mobile aggregate of a variety of substances that occludes the vasculature. Sources of emboli include clots, air, amniotic
fluid, bacteria, fat, and foreign matter. These emboli cause ischemia and necrosis when a vessel is
totally blocked.
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disorders of arteries
9. An aneurysm is a localized dilation of a vessel wall; the aorta is particularly susceptible.
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disorders of arteries
8. The clinical manifestations of OH include fainting and may involve cardiovascular symptoms, as well as impotence and bowel and bladder dysfunction.
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disorders of arteries
1. The most common source of arterial emboli is the heart as a result of mitral and aortic valvular
disease and atrial fibrillation, followed by myxomas. Tissues affected include the lower
extremities, the brain, and the heart.
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disorders of arteries
12. Emboli to the central organs cause tissue death in lungs, kidneys, and mesentery.
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disorders of arteries
13. Peripheral vascular diseases include Buerger's disease and Raynaud phenomenon, involving
arterioles of the extremities.
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disorders of arteries
14. Atherosclerosis is a form of arteriosclerosis and is the leading contributor to coronary artery
disease (CAD) and cerebrovascular disease.
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disorders of arteries
15. Atherosclerosis is an inflammatory disease that begins with endothelial injury.
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disorders of arteries
16. Important steps in atherogenesis include vasoconstriction, adherence of macrophages, release of
inflammatory mediators, oxidation of low-density lipoprotein, formation of foam cells and fatty
streaks, and development of fibrous plaque.
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disorders of arteries
17. Once a plaque has formed, it can rupture, resulting in clot formation and instability and
vasoconstriction, which lead to obstruction of the lumen and inadequate oxygen delivery to
tissues.
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disorders of arteries
18. Ischemic heart disease is most commonly the result of CAD and the ensuing decrease in
myocardial blood supply.
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disorders of arteries
19. Peripheral artery disease is the result of atherosclerotic plaque formation in the arteries that
supply the extremities, and it causes pain and ischemic changes in the nerves, muscles, and skin
of the affected limb.
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disorders of arteries
31. Treatment of an MI includes revascularization (thrombolytics or PCI) and administration of
antithrombotics, angiotensin-converting enzyme (ACE) inhibitors, and beta-blockers. Pain relief and fluid management also are key components of care.
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disorders of arteries
20. CAD is the result of an atherosclerotic plaque that gradually narrows the coronary arteries or that
ruptures and causes sudden thrombus formation.
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disorders of arteries
21. Many risk factors contribute to the onset and escalation of CAD, including traditional risk factors
such as dyslipidemia, cigarette smoking, hypertension, diabetes mellitus (insulin resistance), obesity, and sedentary lifestyle, and nontraditional risk factors such as elevated C-reactive protein levels, hyperhomocysteinemia, and changes in adpokines
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disorders of arteries
22. Atherosclerotic plaque progression can be gradual and cause stable angina pectoris, which is predictable chest pain caused by myocardial ischemia in response to increased demand (e.g., exercise) without infarction.
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disorders of arteries
23. Prinzmetal angina results from coronary artery vasospasm.
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disorders of arteries
24. Myocardial ischemia may be asymptomatic, which is called silent ischemia, and is a risk factor for
the development of the acute coronary syndromes.
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disorders of arteries
25. Sudden coronary obstruction because of thrombus formation causes the acute coronary
syndromes. These syndromes include unstable angina, non-ST elevation myocardial infarction
(non-STEMI), and ST elevation myocardial infarction (STEMI).
26. Unstable angina results in reversible myocardial ischemia.
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disorders of arteries
29. MI is clinically classified as non-STEMI or STEMI based on electrocardiographic findings that
suggest the extent of myocardial damage (subendocardial versus transmural).
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disorders of arteries
28. Dysrhythmias and cardiac failure are the most common complications of acute MI.
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disorders of arteries
27. Myocardial infarction (MI) is caused by prolonged, unrelieved ischemia that interrupts blood
supply to the myocardium. After about 20 minutes of myocardial ischemia, irreversible hypoxic
injury causes cellular death and tissue necrosis.
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disorders of arteries
26. Unstable angina results in reversible myocardial ischemia.
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disorders of arteries
30. An increase in plasma enzyme levels is used to diagnose the occurrence of MI as well as indicate
its severity. Elevations of the isoenzymes creatine kinase-myocardial bound (CK-MB), troponins,
and lactate dehydrogenase 1 (LDH-1) are most predictive of an MI.
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disorders of heart wall
1. Inflammation of the pericardium, or pericarditis, may result from several sources (e.g., infection, trauma or surgery, neoplasm). Pericarditis presents with symptoms that are physically troublesome, but in and of themselves they are not life-threatening.
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disorders of heart wall
2. Fluid may collect within the pericardial sac (pericardial effusion). Cardiac function may be severely impaired if the accumulation of fluid occurs rapidly and involves a large volume
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disorders of heart wall
3. Cardiomyopathies are a diverse group of primary myocardial disorders that are usually the result
of remodelling, neurohumoral responses, and hypertension. The cardiomyopathies are categorized as dilated (formerly, congestive), hypertrophic (asymmetric), or restrictive (rigid and noncompliant). The size of the cardiac muscle walls and chambers may increase or decrease depending on the type of cardiomyopathy, thereby altering contractile activity.
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disorders of heart wall
4. The hemodynamic integrity of the cardiovascular system depends to a great extent on properly functioning cardiac valves. Congenital or acquired disorders that result in stenosis, regurgitation, or both can structurally alter the valves.
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disorders of heart wall
5. Characteristic heart sounds, cardiac murmurs, and systemic complaints assist in identification of an abnormal valve. If severely compromised function exists, a prosthetic heart valve may be surgically implanted to replace the faulty one.
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disorders of heart wall
10. Human immunodeficiency virus (HIV) infection and acquired immune deficiency syndrome (AIDS) are associated with cardiac abnormalities, including myocarditis, endocarditis, pericarditis, and cardiomyopathy.
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disorders of heart wall
9. Infective endocarditis is a general term for infection and inflammation of the endocardium, especially the cardiac valves. In the mildest cases, valvular function may be slightly impaired by vegetations that collect on the valve leaflets. If left unchecked, severe valve abnormalities, chronic bacteremia, and systemic emboli may occur as vegetations detach from the valve surface and travel through the bloodstream. Antibiotic therapy can limit the extension of this disease.
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disorders of heart wall
6. Mitral valve prolapse syndrome (MVPS) describes the condition in which the mitral valve leaflets do not position themselves properly during systole. MVPS may be a completely asymptomatic condition or can result in unpredictable symptoms.
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disorders of heart wall
7. Rheumatic fever is an inflammatory disease that results from a delayed immune response to a streptococcal infection in genetically predisposed individuals. The disorder usually resolves without sequelae if treated early.
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disorders of heart wall
8. Severe or untreated cases of rheumatic fever may progress to rheumatic heart disease, a potentially disabling cardiovascular disorder.
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Manifestations of Heart Disease
1. Heart failure (HF) can be divided into HF with reduced ejection fraction (systolic) and HF with preserved ejection fraction (diastolic).
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heart disease
2. The most common causes of left ventricular failure are MI and hypertension.
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heart disease
3. HF with reduced ejection fraction (systolic) is caused by increased preload, decreased contractility, or increased afterload. These processes result in an increased left ventricular end-diastolic volume
and an increased left ventricular end-diastolic pressure (LVEDP) that cause increased pulmonary
venous pressures and pulmonary edema.
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heart disease
4. In addition to the hemodynamic changes of left ventricular failure, there is a neuroendocrine
response that tends to exacerbate and perpetuate the condition.
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heart disease
5. The neuroendocrine mediators of HF include the SNS and the RAAS; thus diuretics, beta-blockers,
and ACE inhibitors are important components of pharmacological therapy.
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heart disease
6. HF with preserved ejection fraction (diastolic HF) is a clinical syndrome characterized by the
symptoms and signs of HF, a preserved ejection fraction, and abnormal diastolic function.
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heart disease
7. Diastolic dysfunction means that the LVEDP is increased, even if volume and cardiac output are
normal.
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heart disease
8. Right ventricular failure can result from left ventricular failure or pulmonary disease.
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heart disease
9. A dysrhythmia (arrhythmia) is a disturbance of heart rhythm. Dysrhythmias range in severity
from occasional missed beats or rapid beats to disturbances that impair myocardial contractility
and are life-threatening.
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heart disease
10. Dysrhythmias can occur because of an abnormal rate of impulse generation or an abnormal
conduction of impulses.
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