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105 Cards in this Set
- Front
- Back
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Describe the layers of the pericardium
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The pericardium is the outer covering of the heart.
Outer to inner layers include: a. pericardial sac - consists of fibrous pericardium – outer layer of connective tissue – anchors pericardium to great veins and arteries, sternum, and diaphragm. The serous membrane lining inner surface of fibrous pericardium is called the parietal pericardium b. pericardial space – filled with pericardial fluid, between parietal pericardium and visceral pericardium c. visceral pericardium/epicardium – serous membrane covering the heart surface |
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Describe the organization of the myocardium.
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The myocardium is the cardiac muscle tissue
forming walls of atria and ventricles. Muscle fibers are anchored to fibrous connective tissue between atria and ventricles. Fibers are in a “swirled” arrangement that contract atria and ventricles in a “wringing” movement. Fibers circling both atria are continuous and integrated, and fibers circling both ventricles are also continuous and integrated, so that both atria pump at same time, and both ventricles pump at same time |
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Describe the flow of blood through the heart...
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The right atrium receives blood from superior
and inferior vena cava and coronary sinus, pumps it through tricuspid valve to right ventricle. Right ventricle pumps blood through pulmonary semilunar valve into pulmonary trunk, blood flows through pulmonary arteries to lungs. Left atrium receives blood from lungs via pulmonary veins, pumps it through mitral valve to left ventricle. Left ventricle pumps blood through aortic semilunar valve to aorta and systemic arteries. |
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Describe normal heart valves.
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The cardiac valves prevent backflow of blood, allow blood to flow only in one direction. They are not active structures, they react passively to pressure.
The valve leaflets are thin layers of connective tissue covered by endothelium that is continuous with endocardium. The annuli fibrosi are fibrous rings enclosing heart valves, prevent valve openings from becoming dilated when blood is forced through during heart contractions, andprovide firm base for effective valve closure during heart relaxation. |
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Where are the atrioventricular (AV) valves?
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tricuspid on right side, bicuspid/mitral on left side
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How are the AV valves are prevented from eversion (opening backward so that some blood
would flow backward from ventricle to atrium)? |
They are anchored to chordae tendinae,
which are in turn anchored to papillary muscles (Small extensions from ventricular myocardium) This prevents backflow of blood from ventricles to atria. |
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Where are the semilunar (SL) valves?
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The pulmonary semilunar is between right ventricle and
pulmonary trunk, aortic semilunar between left ventricle and aorta. Both valves have three leaflets. |
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Is eversion a possibility with the semilunar valves?
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No, the smaller lumen of the blood vessels and
strength of annuli fibrosi prevent backflow of blood through these valves (structures like chordae tendinae are not needed) |
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Systole
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Contraction of ventricles
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Diastole
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Relaxation of the ventricles
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End diastole volume (edv)
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volume of blood in ventricle at end of diastolic filling period
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Stroke volume (sv)
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volume of blood pumped from a ventricle SV = EDV -ESV
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End systolic volume (esv)
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volume of blood remaining in the ventricle after systole
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Ejection fraction (ev)
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% of blood pumped from filled ventricle EF = SV/EDV x 100%
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Cardiac output (co)
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volume of blood pumped from left ventricle per minute
CO (ml/min) = HR (beats/min) X SV (ml/beat) |
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How is heart rate controlled by the nervous system?
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The sinoatrial node (SA) node is
pacemaker of heart, has fastest automatic rhythm. Rate of firing is modified by sympathetic nervous system (beta-1 receptors, increases HR) and parasympathetic nervous system (muscarinic receptors, decreases HR) |
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Describe the electrical conduction pathway of the heart
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From SA node, impulses pass to
atrial conducting network, then to atrial muscle cells, which contract, and also to the atrioventricular (AV) node, which provides a time delay - from AV node impulses pass to bundle of His, to Purkinje fibers, to ventricular muscle cells, which contract. |
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What is an ectopic focus?
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An ectopic focus is an abnormal pacemaker, generates electrical
impulses, can have minor effects to major effects |
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P wave represents
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Atrial depolarization which leads to atrial contraction
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Qrs complex
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Ventricular depolarization which leads to ventricular contraction
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Pv interval
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Indicates rate of passage of impulses through av node
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T wave
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Ventricular repolarization
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Qt interval
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indicates duration of ventricular action potentials, most of QT interval is absolute refractory period, during which ventricles cannot be restimulated, prolonged QT interval is dangerous since there is a longer relative refractory period, during which ventricles could be restimulated, could lead to cardiac arrhythmia
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Sinus arrhythmias originate where? Give the two examples :
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Sa node, sinus tach and sinus brady
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What type of arrhythmias are supra ventricular arrhythmias? Give the examples...
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These are atrial arrhythmias - abnormal P waves, normal QRS
complex – these include paroxysmal supraventricular tachycardia (PSVT's), pr emature atrial contractions (PAC,s), atrial flutter, atrial fibrillation |
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What is an av block?
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Slowing or prevention of impulses through the av node
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A 1st degree av block has what distinguishing factors?
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Increased pr interval
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2nd degree av block will have
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2,3,4 p waves for every qrs
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Describe 3rd degree av block
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There is a total block, there is no relationship between the p waves and the qrs interval, pacemaker is now in the ventricles
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Describe ventricular arrhythmias
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originating in ventricles - wide or odd-shaped QRS complex, possibly inverted T wave – these include premature ventricular contractions (PVC's), ventricular flutter, ventricular fibrillation.
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Pv interval
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Indicates rate of passage of impulses through av node
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T wave
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Ventricular repolarization
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Qt interval
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indicates duration of ventricular action potentials, most of QT interval is absolute refractory period, during which ventricles cannot be restimulated, prolonged QT interval is dangerous since there is a longer relative refractory period, during which ventricles could be restimulated, could lead to cardiac arrhythmia
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Sinus arrhythmias originate where? Give the two examples :
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Sa node, sinus tach and sinus brady
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What type of arrhythmias are supra ventricular arrhythmias? Give the examples...
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These are atrial arrhythmias - abnormal P waves, normal QRS
complex – these include paroxysmal supraventricular tachycardia (PSVT's), pr emature atrial contractions (PAC,s), atrial flutter, atrial fibrillation |
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What is an av block?
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Slowing or prevention of impulses through the av node
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A 1st degree av block has what distinguishing factors?
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Increased pr interval
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2nd degree av block will have
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2,3,4 p waves for every qrs
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Describe 3rd degree av block
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There is a total block, there is no relationship between the p waves and the qrs interval, pacemaker is now in the ventricles
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Describe ventricular arrhythmias
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originating in ventricles - wide or odd-shaped QRS complex, possibly inverted T wave – these include premature ventricular contractions (PVC's), ventricular flutter, ventricular fibrillation.
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How does the parasympathetic nervous system ("rest and digest") affect heart function?
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Parasympathetic nervous system innervates SA and AV nodes, vagus nerve releases
acetylcholine (ACh) to stimulate muscarinic receptors on SA node cells - slows HR (negative chronotropic effect), also stimulates muscarinic receptors on AV node cells - slows conduction through AV node (negative dromotropic effect) These effects will lower BP. |
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How does the sympathetic nervous system affect the blood vessels of the body?
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Sympathetic nervous system constricts peripheral blood vessels and dilates blood vessels in vital organs.
a. Sympathetic system innervates smooth muscle of peripheral blood vessels – norepinephrine (NE) stimulates alpha-1 receptors on smooth muscle cells so that they contract à peripheral vasoconstriction, increased TPR – this effect will raise BP b. sympathetic nervous system also innervates smooth muscle of blood vessels in vital organs – norepinephrine (NE) stimulates beta-2 receptors on smooth muscle cells so that they relax à vasodilation in brain, heart, skeletal muscle to increase blood supply to these organs – this effect will slightly decrease BP |
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How does epi affect the heart?
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Epinephrine (EPI) released by adrenal medulla
assists the sympathetic nervous system, since EPI also stimulates alpha-1, beta-1, and beta-2 receptors |
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What three variables determine stroke volume?
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a. EDV, which is called preload
b. resistance by arteries to emptying of ventricles, which is called afterload c. myocardial contractility (this is correct term for this specific variable, “force of contraction” is a more general term) |
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Define edv aka preload
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This is volume of blood filling the ventricles after diastole. This volume determines how much “stretching” of the myocardium occurs. Preload is determined by venous return to heart - depends on blood volume and venous constriction or dilation –
constricted veins mean more blood is delivered to heart, greater preload; dilated veins mean that blood pools in veins, less blood is delivered to heart, lesser preload. |
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What is the Franks-Starling Law of the Heart and how does it relate to preload?
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This law describes the relationship of preload to stroke volume. This “law” states that the greater the EDV/preload, the greater the stretching of the myocardium, the better the interactions between actin and myosin in cardiac muscle, and the greater the force of contraction of the ventricle -à the greater the stroke volume. This increased stroke volume with increased preload is called intrinsic regulation of stroke volume. However, if preload is too great àstretching is too great, actin and myosin do not interact wellà poor force of contraction, heart will begin to fail.
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Define and describe afterload
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Afterload is the resistance by arteries to emptying of ventricles –depends on blood viscosity and constriction or dilation of arteries, also precapillary sphincters.
Afterload is greater if greater blood viscosity, constricted arteries, constricted precapillary sphincters. Afterload is lesser if lesser blood viscosity, dilated arteries, dilated precapillary sphincters. |
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Define and describe myocardial contractility....
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This is the intrinsic ability to contract or intrinsic “tension” of the myocardium that is independent of starting tension (does not depend on EDV/preload) – depends on structural organization of cardiac cells and metabolic state.
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Where are the major coronary arteries?
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Left coronary artery arises from aorta – 2 branches :
left anterior descending artery (LAD) – descends anteriorly (front of heart) between right and left ventricles and circumflex artery (CX) – travels between left atrium and left ventricle around toward posterior and apex on left side. Right coronary artery arises from aorta – travels between right atrium and right ventricle around toward posterior and apex on right side. |
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Why does most blood flow to the myocardium during diastole?
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This is because of compression of myocardium during systole, 60% of blood flow to myocardium takes place through left coronary artery to blood vessels inside of myocardium during diastole.
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Why may the surface arteries of the heart be more susceptible to "wear and tear" and therefore atheroscerosis?
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Surface cardiac arteries, including the major coronary arteries, fill maximally during systole, since they are on the surface and are not compressed.
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What causes the coronary arteries to dilate and increase blood supply when the heart is very active?
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Intensely active myocardium produces and uses much ATP, resulting in adenosine as a breakdown product - adenosine causes production of nitric oxide (NO)(also called endothelial derived relaxing factor (EDRF)), which dilates the coronary arteries. Other factors that cause increased NO production are histamine, bradykinins, ACh from very active skeletal muscle.
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What causes the coronary arteries to constrict when necessary?
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Endothelin-1 (ET-1) is a powerful vasoconstrictor – constricts coronary arteries when necessary.
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List possible causes of heart failure....
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weakened myocardium due to IHD and/or HTN, arrhythmias, restrictions to filling and pumping, damaged heart valves, anemia, hyperthyroidism
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When is the cause of death considered heart failure?
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If despite adequate venous filling, ventricles still cannot adequately pump blood to nourish vital organs to sustain life – cause of death is HF. If HF is due to another disease process (cancer, blood loss, etc.) – cause of death is considered to be the other disease process.
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What is chronic v acute heart failure?
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a. acute – develops quickly (as after MI), a few seconds to a few days
b. chronic – develops gradually, usual cause is ischemic heart disease (myocardium is deprived of nutrients and becomes damaged) and/or HTN (myocardium becomes damaged due to years of overwork). Chronic HF can predispose to acute HF. Usually left ventricle (LV) fails first, due to greater workload. |
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What are the consequences and symptoms of left ventricle failure?
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a. blood backs up in lungs à SOB, pulmonary congestion, pulmonary edema, “bloody” cough
b. decreased perfusion of brain àcerebral hypoxia à CNS symptoms c. decreased perfusion of kidneys à activation of RAA à angiotensin II, which has 3 important effects - vasoconstriction (increases afterload), Na+ and water retention (leads to increased preload, edema), and remodeling of heart structure. d. LVF eventually will lead to right ventricular failure (RVF) |
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What causes right ventricle failure?
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RVF occurs when RV must pump against high resistance/congestion in lungs – usual cause of this lung congestion is LVF. RVF can also be caused by lung diseases such as chronic bronchitis and emphysema.
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What are the consequences and symptoms of right ventricle failure?
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a. blood backs up in systemic veins, “waiting” to be pumped, leads to a pattern of symptoms called “cor pulmonale” – hepatomegaly, splenomegaly, congestion in kidneys (greater reduction in perfusion than with LVF)
b. congestion in kidneys leads to greater activation of RAA à angiotensin II, which has 3 important effects - vasoconstriction (increases afterload), Na+ and water retention (leads to increased preload, edema), remodeling of heart structure c. congestion in kidneys also leads to reduced kidney function à azotemia d. RVF eventually will lead to LVF. |
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What is low output heart failure?
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This is the usual case in HF, as with damage to myocardium. There is compensatory increase in HR in failing heart, but still low CO (due to decreased SV) à impaired circulation and systemic vasoconstriction à cold, pale, cyanotic extremities
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What is high output heart failure?
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This is HF caused by high demand on heart in some diseases, such as anemia or hyperthyroidism. Increased demand increases HR and SV which increases CO à warm, flushed extremities. If heart cannot maintain high CO, then HF will occur, called high-output HF.
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What is acute pericardititis and what are it's clinical symptoms?
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a. acute pericarditis is nonspecific inflammation of pericardium in response to injury – usually resolves with minimal consequences, but can lead to chronic pericarditis b. clinical symptoms – acute onset of constant chest pain which decreases when sitting or leaning forward, friction rub upon auscultation, if extensive pericardial effusion - diminished heart sounds and possible cardiac tampondae which lowers CO
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What types of pericardial effusion can happen with acute pericarditis?
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a. fluid in pericardial space has protein/fibrin content - may be serous, serofibrinous, fibrinous – the more fibrin content, the greater the risk of roughening of pericardium and adhesions – usually resolves well
b. purulent suppurative effusion – fluid in pericardial space is pus - much more serious – due to bacterial or viral infectionb |
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What are the consequences of pericardial effusion which results from acute pericarditis?
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1)fibrous obliteration of pericardial cavity – occurs often
2) adhesions between visceral and parietal pericardium, also adhesions to adjacent structures 3) above problems cause restriction of ventricles in systole and diastole |
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What are the causes of acute pericarditis?
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intrinsic heart disease, disease in adjacent structures, systemic diseases, tuberculosis (TB) pericarditis, acute idiopathic pericarditis (probably viral)
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What is chronic constrictive pericarditis and what are the consequences?
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In chronic constrictive pericarditis there is excessive fibrosis à dense and diffuse scarring of pericardial sac à nonelastic “shell” encasing heart which can become calcified in 50% of cases. Calcified shell condition is called “concreto cordis”. The shell encasing the heart can cause stenosis of large vein entry points to right atrium à restricted venous return à hepatomegaly, splenomegaly, decreased EDV/preload with decreased CO
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What is the treatment for severe cases of chronic constrictive pericarditis?
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Surgical removal of the visceral and parietal pericardium
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What is myocarditis?
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Inflammation of the myocardium
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What are the causes of myocarditis?
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1) usually secondary to another disease, such as viral infection (most common cause, usually Coxsackie B virus) , bacterial infection, protozoal infection, parasitic infection, hypersensitivity, trauma
2) sometimes primary at focal sites –idiopathic (cause unknown) |
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What are the consequences of myocarditis?
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1) usually mild with complete resolution
2) sometimes necrosis of cardiac muscle cells which can lead to HF |
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Describe viral myocarditis...
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This is usually caused by Coxsackie B virus in infants and young men (especially in confined living/working areas) There is fluid exudate into pericardial sac and infiltration of inflammatory cells into myocardium. Consequences are usually mild in adults, more severe in immunosuppressed, fetus, newborns. Clinical symptoms include pericardial pain, weakness, fatigue, malaise, fever, dyspnea, tachycardia, and AV valve dysfunction. The clinical course is variable – usually resolves in 1 to 2 months, but can cause chronic HF, and rarely, acute HF.
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What is Chagas’disease?
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Chagas’disease is myocarditis caused by infection with a protozoa, Trypansoma, mainly seen in South America and South Africa.
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What are the causes of Infective Endocarditis (IE), and which form is more severe?
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a. the cause is usually bacterial (especially Staphylococcus or Streptococcus species), sometimes atypical bacteria (especially Rickettsiae species), sometimes fungal. b. Acute form is more serious than subacute - 60 to 80% mortality rate for acute, 5 to 10% mortality rate for subacute. |
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What are the causes of acute infective endocarditis?
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cause – usually preexisting infection with Staphylococcus aureus or a Streptococcus species, usually no preexisting heart disease, IV drug use is a risk factor
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What are the symptoms of acute infective pericarditis?
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symptoms – changing heart murmur, high fever, shaking chills, splinter hemorrhages, splenomegaly, hematuria
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What is the clinical course for acute infective endocarditis?
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clinical course – bacterial infection of valve à thrombus “vegetation” formation à death within 2 weeks if untreated due to HF or emboli
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What is the cause of subacute infective endocarditis?
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usually preexisting heart condition, sometimes after cardiac surgery including valve replacement – microorganisms colonize preexisting thrombi in heart
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What are the symptoms of subacute infective endocarditis?
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symptoms – vague - fever, anemia, debilitation, malaise, splinter hemorrhages, splenomegaly
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What is the clinical course of subacute infective endocarditis?
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Disease develops slowly over 3-6 months
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How can subacute infective endocarditis be prevented?
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In patients with heart problems – prophylaxis with antibiotics before and possibly after potentially infective procedure such as dental work.
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Describe valvular stenosis...
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narrowing of a heart valve so that forward flow of blood is restricted
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What are the causes of valvular stenosis?
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Rheumatic heart disease and infective endocarditis
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What are e consequences of valvular stenosis?
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1) narrow valves cause congestion upstream of problem
– in heart chambers and/or blood vessels à HTN in affected vessels 2) usually no HTN in downstream blood vessels due to compensatory mechanisms 3) abnormal blood flow causes abnormal heart sounds – heart murmurs |
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What are the consequences of mitral valve stenosis?
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consequences:
Narrowed mitral valve causes impaired filling of LV à dilation of LA à hypertrophy of LA with possible compression of esophagus. Also, blood backs up in lungs à lung congestion à RVF |
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What are the symptoms of mitral valve stenosis?
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symptoms:
1) diastolic murmur with snapping sound 2) with severe stenosis less oxygenated blood is pumped by LV to systemic arteries à cyanosis and fatigue 3) with severe stenosis compression of esophagus à dysphagia 4) with severe stenosis RVF à reduced CO à dizziness, syncope, fatigue, pallor, reduced pulse pressure |
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What are the consequences of aortic valve stenosis?
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Narrowed aortic valve increases afterload for LV à hypertrophy of LV à increased risk of ischemia, angina à eventual HF
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What are the symptoms of aortic valve stenosis?
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1) systolic murmur
2) decreased CO à dizziness, syncope, fatigue, pallor, reduced pulse pressure 3) later with severe condition –pulmonary congestion |
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Describe valvular insufficiency/incompetence...
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In this situation, a damaged valve permits a back flow of blood, usually 40 to 50% of the volume regurgitates, although CO is maintained by increased SV, (due to increased preload by Frank-Starling mechanism), eventually preload is too great à dilation and failure of affected ventricle.
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Causes of mitral valve insufficiency...
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LV infarct à rupture of papillary muscle, RHD or IE à rupture of chordae tendonae
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Consequences of mitral valve insufficiency...
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left atrium fills with blood from lungs and also regurgitated blood from LV (backflow through mitral valve) à dilation of LA à backup of blood in lungs à congestion, pulmonary HTN, other lung problems, LV hypertrophy, LA hypertrophy is also possible
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Symptoms of mitral valve insufficiency...
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1) systolic heart murmur
2) dyspnea 3)early - near normal CO due to Frank-Starling law, later with LVF – reduced CO à dizziness, syncope, fatigue, pallor, reduced pulse pressure |
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What is mitral valve prolapse?
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Occurs in 5% of population, abnormality of valve leaflets and chordae tendinae – systolic heart murmur but usually no significant problems
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Causes of aortic valve insufficiency...
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causes – perforated leaflets due to infection or inflammation, impairment of valve closure due to scarring
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Symptoms of aortic valve insufficiency...
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symptoms – regurgitation of blood causes diastolic heart murmur; altered hemodynamicsà increased pulse pressure, syncope, dizziness, pounding headaches weakness, fatigue
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Consequences of aortic valve insufficiency...
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consequences - blood regurgitates backward from aorta into LV during diastole à decreased pressure in aorta à altered hemodynamics; eventual LVF
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Stenosis and insufficiency is rarely seen in which heart valves?
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Trcuspid av valve and pulmonic semilunar valve.
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What is rheumatic fever...given symptoms and onset info too...
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This is an inflammatory disease – affects iheart, skin, serosa, blood vessels, lungs, joints
a. usually starts with streptococcal pharyngitis, RF 1 to 4 weeks later if no treatment b. first attack between ages 5 to 15, equal incidence in boys and girls c. symptoms; if sudden - with fever, sore joints, tachycardia if mild - fever, malaise |
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Stenosis and insufficiency is rarely seen in which heart valves?
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Trcuspid av valve and pulmonic semilunar valve.
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What is rheumatic heart disease?
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RHD occurs when cardiac effects of RF become serious, more likely in younger patients.
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What problems can rheumatic heart disease cause?
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1) usually valve damage à can lead to HF and death;
2) sometimes affects pericardium, myocardium, endocardium or combination of these sites |
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What is rheumatic fever...given symptoms and onset info too...
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This is an inflammatory disease – affects iheart, skin, serosa, blood vessels, lungs, joints
a. usually starts with streptococcal pharyngitis, RF 1 to 4 weeks later if no treatment b. first attack between ages 5 to 15, equal incidence in boys and girls c. symptoms; if sudden - with fever, sore joints, tachycardia if mild - fever, malaise |
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What is rheumatic heart disease?
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RHD occurs when cardiac effects of RF become serious, more likely in younger patients.
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What is the pathogenesis of rheumatic fever and rheumatic heart disease?
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Pathogenesis is not well understood. it is believed that GABHS antigen is similar to a self-antigen à Ab attack Strep and own body cells à damaged cells release histamine, kinins à inflammation
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What problems can rheumatic heart disease cause?
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1) usually valve damage à can lead to HF and death;
2) sometimes affects pericardium, myocardium, endocardium or combination of these sites |
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What is the pathogenesis of rheumatic fever and rheumatic heart disease?
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Pathogenesis is not well understood. it is believed that GABHS antigen is similar to a self-antigen à Ab attack Strep and own body cells à damaged cells release histamine, kinins à inflammation
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