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117 Cards in this Set
- Front
- Back
single layer of epithelial cells of the heart (outermost)
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epicardium
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layer of cardiac myocytes and connective tissue (middle layer)
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myocardium
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single layer of endothelial cells (inside layer)
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endocardium
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the sac the heart sits in; composed of connective tissue with a few ml of fluid for lubrication
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pericardial sac
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when fluid collects inside the sac and the heart cannot fill or pump
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cardiac tamponade
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these allow for the unidirectional movement of blood in the heart
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valves
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how do valves open and close?
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pressure differences
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valve that separates the left ventricle and left atria
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mitral (bicuspid)
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valve that separates right ventricle and right atria
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tricuspid
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what holds mitral and tricuspid valve leaflets in place?
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chordae tendineae attached to papillary muscles
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to allow for filling during ventricular relaxation and prevent blood from regurgitating into the atria during ventricular contraction
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Purpose of mitral and tricuspid valves
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why are the papillary muscle cells among the first to depolarize?
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to tense the valve to prevent the valve from failing during ventricular contraction
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during heart contraction, these allow blood to move from the ventricles into the pulmonary trunk and aorta;
during relaxation they prevent blood from moving back into ventricles |
semilunar valves
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During ventricular contraction when the semilunar valves open, why do their leaflets flap over the openings to the coronary arteries?
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to prevent blood from entering during ventricular contraction because the pressure is too high; coronary arteries receive their blood during ventricular relaxation when semilunar valves are in the closed position
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Striated muscle fibers associated with the heart; have actin and myosin arranged in sarcomeres; cells are shorter, branched, and have a single nucleus
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myocardium
*a cardiac muscle fiber is made up of many individual cells (not one cell, like skeletal muscle) |
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individual cells joined together to form a fiber or disc with numerous gap junctions
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intercalated disc
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what is the purpose of gap junctions in the myocardium?
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electrical events in one cell are transmitted to others by means of gap junctions; AP in one cell can influence other cells and thus propagate from cell to cell throughout the heart by means of the gap junctions
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Does the heart beat at a constant rate and volume?
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no
-Heart is highly regulated. -Rich neural innervation -Responds to hormones. |
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these nerves release norepinephrine
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sympathetic fibers
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the receptors that norepinephrine and epinephrine bind to
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beta-adrenergic receptors
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this hormone is from the adrenal medulla, binds to the same recetors, thus acting like norepinephrine
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epinephrine
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what is the net result of beta-adrenergic receptor binding of norepinephrine/epinephrine?
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increased heart rate and force of contraction
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these neurons release acetylcholine
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parasympathetic fibers
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what does acetylcholine do?
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binds to receptors that slow the heart
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these drugs bind and block beta adrenergic receptors
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beta blockers
-slow heart rate and reduce force of contraction |
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Why would it be a poor design to deliver blood to the heart muscle directly from the left ventricle?
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too much pressure and coronary arteries would have to be huge
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1.to provide a uniform and abundant blood supply to the myocardium
2.to deliver oxygen, nutrients, remove CO2 and other waste products |
purpose of coronary circulation
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results in more than one artery perfusing the same tissue
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anastomoses
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the leading cause of death in the US
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coronary artery disease
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what causes coronary artery disease (cardivascular disease)?
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atherosclerosis
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begins at an early age and develops over many years and considered a chronic inflammatory disease
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atherosclerosis
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modifiable:
high fat diet high serum cholesterol (<160 mg/dL considered good) high LDL low HDL smoking (increased fibrinogen levels in smokers, increases LDL and decreases HDL) hypertension - especially elevated systolic pressure stress, sedentary lifestyle, obesity, diabetes nonmodifiable age sex differences racial differences - low in Asians - probably due to diet genetic differences |
risk factors associated with CAD (CVD)
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this is white, elevated and partially blocks the lumen - occur at bifurcations, curvatures, and at narrowings
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plaque
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these are thought to develop into plaque
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fatty streaks
*fatty streak formation can start as early as 10 |
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-occurs with 75% blockage of coronary artery
-ischemia and angina pectoris |
first appearance of symptoms of CAD
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1.if severe ischemia occurs,
2.necrosis of the myocardium results (MI) 3.plaques may become hemorrhagic 4.lead to thrombosis or 3.plaques may calcify(dystrophic-causes inflammation from an area of unresolved healing) 4.core of plaque becomes necrotic, ruptures, and leads to thrombosis |
pathogenesis of CAD
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If a thrombus blocks the artery it can result in
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sudden unstable angina or an MI
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If a thrombus embolizes and blocks the coronary artery at a more distal site, this is called
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acute coronary syndrome
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1.drug Tx: nitroglycerin, beta blockers
2.CABG 3.angioplasty |
treatment of CAD to restore blood flow
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dilates arteries and reduce peripheral resistance
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nitroglycerin (nitric oxide)
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this drug reduces work load on the heart
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beta blockers (slows heart and force of contraction)
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these drugs prevent thrombosis
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Ca channel blockers
aspirin |
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-a less invasive procedure
-quick recovery -local anesthesia insert a catheter into the femoral, brachial, or carotid artery and snake it to coronary artery openings at base of aorta, cath. w/baloon pushes plaques against vessel wall, sometimes a stent is placed to prevent restenosis |
angioplasty
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-much more invasive
-major surgery through the sternum and opening of the pericardium and stopping the heart -venous or arterial graft from leg -sewn into the aorta and bypasses the blockage to the artery to restor blood supply distal to the blockage |
CABG
coronary artery bypass graft (bypass surgery) |
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conditions which results when the blood supply is not able to meet metabolic demands of myocardium
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inschemic heart disease (aka mycardial ischemia)
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angina pectoris and myocardial infarction
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symptoms of ischemic heart disease
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Perception of pain in ischemic heart disease is thought to be related to what mechanism?
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Lactic acid, the waste product of the glycolytic pathway to produce ATP, builds up when oxygen is not available and stimulates nerve endings.
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Where is pain perceived from ischemic heart disease?
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Angina or MI pain:
substernal, feeling of tightness, crushing pain, may radiate down one or both arms into neck and jaw pallow, dyspnea, profuse sweating in women: fatigue |
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means "to choke"
refers to chest pain or pressure associated with myocardial ischemia radiates to jaw and left arm ("referred pain" travels common neurons from these areas) |
Angina
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what are the three kinds of angina?
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classic angina
variant angina unstable angina |
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-occurs in people with CAD in which exertion above normal activity increases metabolic needs of the heart, but demand exceeds supply
-with rest or vasodilator, chest pain diminishes (myocardial demand decreases) |
classic angina (exertional, stable)
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In an otherwise healthy individual,this results from coronary artery spasm (constriction) that results in myocardial ischemia; usually at night or at rest
-may occur in people without any evidence of CAD -may occur in people who can run a mile without difficulty unknown mechanism |
variant angina (atypical)
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-Occurs in people with a prior history of classic angina in which the pain does not subside at rest
-Occurs in people with a prior history of classic angina with activity which in the past did not result in angina -or angina occurs even at rest |
unstable angina
*a worsening of the normal pattern of angina pain |
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ischemic necrosis of myocardium, n usually results from prolonged ischemia - 20-40 minutes (depends on the amount of anastomoses).
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Myocardial Infarction (MI)
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this is influence by the extent, severity, and duration of ischemmic episode and the metabolic needs of the myocardium at the time of the event
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size of infarct
*the larger the infarct the greater the loss of contractility |
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why do infarcts usually occur in the left ventricle?
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left ventricle works the hardest
*MI results in decreased ventricular function |
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1.central area of necrosis
2.surrounded by an area of injury 3.which is surrounded by an area of ischemia |
the sum of 1-3 determines amount or area of myocardial dysfunction from an MI
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area of necrosis from MI is replaced by what?
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scar tissue, since cardiac myocytes cannot regenerate
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what is the significance of the negative impact of scar tissue in the myocardium?
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scar inhibits tissue contractility and the significance of this depends on the amount of scar tissue formed; as contractility falls, heart failure ensues
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what are the compensatory mechanisms initiated to maintain cardiac output?
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peripheral vascular constriction
heart rate increase renal retention of sodium and water activation of renin-angiotensin system |
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-these range from sudden death to dysrhythmias, ventricular rupture, to no symptoms or vague symptoms such as fatigue or acute symptoms
-Acute symptoms include acute substernal pain, diaphoresis, dyspnea, nausea, vomiting, and anxiety |
Clinical Manifestations of a Myocardial Infarction (MI)
*n depends on severity of infarct, previous physical condition, previous infarcts, location of infarct |
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LABS:
-CBC elevated leukocytes -fever -elevated erythrocyte sedimentation rate -myoglobin in serum -Creatine Kinase (CK-MB) -Troponin - (CTnT) |
lab levels indicative of Myocardial Infarction (MI)
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Why is cardia troponin (CTnT) the best marker of the occurence of an MI?
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it is found only in cardiac cells; it is a regulatory protein that mediates contraction in cardiac muscle
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a serum protein released by cells in response to acute injury, infection or other inflammatory stimuli
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C-reactive Protein (CRP)
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why is CRP significant?
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people with athersclerosis make and release CRP, may serve as a predictor of CAD in addition to serum cholesterol levels, especially for people with low cholesterol.
CRP also promotes atherosclerosis formation CRP>3mg/L is considered high risk for CVD |
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diseases in which valve function and the flow of blood through the heart is compromised; accompanied by
-stenosis -cardiac muscle hypertrophy |
valvular disease
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heart valve orifice narrows and leaflets fuse; results in obstruction to blood flow
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stenosis
*chambers try to compensate for stenosis |
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when heart chambers must compensate for stenosis by increasing pressure this leads to a thickening of heart muscle fibers called
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cardiac muscle hypertrophy
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this results from scarring and retraction of the valve leaflets - retrograde flow of blood (regurgitation)
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cadiac insufficiency
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when stenosis and regurgitation occur simultaneously, the defect is called a...
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mixed lesion and is considered to be an advanced disease
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impairment of blood flow from the left atrium to the left ventricle
when valve cannot open during diastole. |
mitral stenosis
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-most common cause - scarring from rheumatic fever
-other cause - congenital stenosis, bacterial endocarditis |
causes of mitral stenosis
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-valve becomes funnel shaped
-rarely any symptoms until the valve orifice is decreased from 4-6 to 1-2 cm -pulmonary symptoms are see first -left atria dilates and hypertrophies |
mitral stenosis
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mitral stenosis leads to
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1.pulmonary edema
2.increased pressure on right heart-right heart hypertrophy 3.progresses to right heart failure |
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if pulmonary hypertension is sufficient to cause blood to exit the pulmonary circuit
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hemoptysis - blood in sputum
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-Rare condition – occurs for the same reasons as mitral stenosis
-5% of all patients with rheumatic fever will develop tricuspid stenosis |
tricuspid stenosis
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Peripheral edema
organomegaly ascities jugular venous distension dyspnea tiredness |
symptoms of right heart failure
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backflow of blood from the left ventricle across the mitral valve to the left atrium during ventricular systole because mitral valve fails to close
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Mitral regurgitation and insufficiency
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common: mitral valve prolapse, coronary artery disease and rheumatic valve disease
less common: include connective tissue disease, papillary muscle dysfunction (why?) and infective endocarditis |
causes of mitral regurgitation and insufficiency
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how is mitral regurgitation and insufficiency diagnosed?
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-no symptoms for many years - then signs of congestive heart failure develop
-systolic murmur -(with rupture of papillary muscle, onset is very rapid, and see sudden onset of pulmonary congestion and pulmonary edema) |
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-rare condition
-backflow of blood from the right ventricle across the tricuspid valve to the right atrium during ventricular systole and tricuspid valve fails to close |
Tricuspid regurgitation
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most common causes of this condition are enlargement of the right ventricle (many causes), rheumatic fever, bacterial endocarditis (IV drug abusers), diet medication called “phen-fen” (dexfenfluramine)
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causes of triscupid regurgitation
*symptoms are the same as tricuspid stenosis |
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-both the conditions of narrowed mitral opening and failure of the mitral valve to close properly caused by rheumatic lesions
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Mixed mitral stenosis and regurgitation
*symptoms are the same as those associated with either mitral stenosis or regurgitation |
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-condition is probably a congenital abnormality (women, or marfan syndrome)caused by a posterior displacement of the posterior cusp of the mitral valve
-large posterior leaflet bulges into the atrium during systole -chordae and papillary muscles become stressed -With time contraction of the papillary muscles decreases and regurgitation may occur as the condition progresses -major complications are bacterial endocarditis or acute mitral insufficiency from chordae stretching and rupture -give antibiotics prior to dental work |
mitral valve prolapse
-patients usually free of symptoms until condition progresses with time |
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obstruction of outflow of blood from left ventricle to the aorta
-obstruction may be at the valve (semilunar), above the valve or below the valve acquired; usually associated with rheumatic fever, degenerative calcific aortic stenosis (dystrophic), and bacterial endocarditis -more common in elderly |
aortic stenosis
*symptoms: chest pain, loss of consciousness, heart failure and pulmonary edema |
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-regurgitation is due to incomplete closure of the aortic semilunar valve
-occurs as a chronic or acute lesion depending on the disease process -chronic lesions include lesions from rheumatic fever, syphilis, hypertension, connective tissue disorders and atherosclerosis -acute lesions can result from aneurysm of the aorta, infectious endocarditis, and rheumatic fever -dissecting aortic aneurysms dilate the valve ring and prevent aortic closure n during systole, blood is ejected into the aorta, but some flows back into the ventricle during diastole -atrial and pulmonary hypertension can develop -Onset of heart failure indicated by fatigue, dyspnea, chest pain, pulmonary |
Aortic regurgitation, insufficiency and incompetence
*Tx: valve replacement |
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-used to be a major cause of valve disease (still is in the 3rd world)
-acute phase -chronic phase occurs in 3% of group A Strep pharyngitis -a hypersensitivity rxn (Type III) - deposit of antibody on antigens, also binds on valves induces inflammatory response -acute: results in tissue damage, necrosis, scarring of mitral and aortic valves -chronic: severe scarring of valves-->stenosis and insufficiency |
Rheumatic fever
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-Infection of the lining of the heart by bacteria(#1), fungi, rickettsiae, viruses and parasites
-Precipitating factors include contaminated needle usage, dental work or endoscopic procedures in persons with previously damaged cardiac valves -Disease progresses very rapidly and causes valvular damage – tricuspid and mitral valves affected the most -damage to the heart valve that results in endothelial damage and exposure of underlying basement membrane and if organisms are in blood they attach to fibrin deposit & proliferate |
Infective endocarditis
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what organism is implicated in infective endocarditis?
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Staph. aureus
*produce friable structures that crumble off --> can embolize and colonize other sites like valve leaflets, peripheral sites |
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what can inflammation from bacterial endocarditis result in?
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malalignment of the valves
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fever, hematuria, fatigue, splenomegaly, petechiae, murmur, weakness, personality changes, memory loss
Osler's node, Janeway's lesions, Roth's spots presents acute and subacute(asymptomatic) |
symptoms of infective carditis
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painful, tender, red, subcutaneous nodules in the pads of the fingers
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Osler's nodes
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flat small irregular nontender red spots on the palms and soles
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Janeway's lesions
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retinal hemorrhages that have a white or yellow center
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Roth's spots
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severe and rapid development of symptoms including high fever, hematuria, fatigue, splenomegaly, petechiae, murmur, weakness, personality changes, memory loss
-could be fatal within days |
Acute Endocarditis
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high IV dose, prolonged antibiotic therapy strong enough to penetrate the vegetation and reach the microorganism because valves have no vasculature - med. must diffuse from blood surrounding it.
-patient given a Picc catheter and antibiotics for 6 weeks or more |
Treatment of Endocarditis
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-initiated by damage to endothelial lining on valve
-damaged areas develop a sterile fibrin deposit -circulating organisms colonize these fibrin deposits -peripheral lesions result from bacterial emboli from the vegetations -emboli can travel and colonize the CNS, pulmonary systems, etc, with the development of symptoms |
pathogenesis of endocarditis
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which organisms are implicated in bacterial endocarditis
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Staphylococcus aureus - pathogen found on skin
– highly virulent – seen in IV drug abusers HACEK group - Haemophilus, Actinobacillus, Cardiobacterium, Eikenella and Kingella – found in the oral cavity and seen following dental work |
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inflammatory processes of the myocardium that results in primary injury to cardiac myocytes
causes: include infections (viral, bacteria, fungi, protozoa and helminths), immune-mediated reactions (rheumatic fever, lupus, transplant rejection) and idiopathic causes |
myocarditis
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Literally means heart muscle disease, but has come to mean heart disease resulting from a primary abnormality in the myocardium, 3 kinds:
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dilated cardiomyopathy
hypertrophic cardiomyopathy restrictive cardiomyopathy |
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most common cause of sudden cardiac death in athletes; autosomal dominant disorder with defects to myosine, tropolyosin, and troponins
-results in enlarged heart w/enlarged left ventricle -basic problem is inability to fill the hypertrophic left ventricle during diastole |
hypertrophic cardiomyopathy
*symptoms are sudden reduce ejection fraction, harsh murmur, exertional dyspnea |
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– Patent ductus arteriosus (PDA)
– Atrial septal defects – Ventricular septal defects – Tetralogy of Fallot – Transposition of the great vessels |
Congenital Heart Diseases-an abnormality of structure or function of the heart, circulatory system or both
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when the the ductus arteriosus doesn't close completely at birth and there is a shunt between aorta and pulmonic arteries
-blood flows from the aorta into pulmonary circulation Dx: 2 weeks postnatally w/harsh murmur -results in increased volume and pressure in the pulmonary system, (followed by CHF) |
Patent ductus arteriosus (PDA)
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fetal opening between atria doesn't close properly
-Right ventricular hypertrophy, respiratory infections, dyspnea, fatigability are seen with larger defects |
atrial septal defects
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-Most common congenital defect
-An opening in the septum that separates the left and right ventricle doesn't close properly -usually requires surgery |
ventricular septal defects
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-Primary cause of cyanotic heart disease
-More common in males -Involves the combination of pulmonary stenosis, ventricular septal defect, and hypertrophy of the right ventricle -polycythemia (compensatory) |
Tetralogy of Fallot
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right & left heart get switched, and right heart cannot maintain systemic circulation
-corrective surgery asap |
Transposition of the great vessels
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inability of the heart to eject blood delivered by the venous system; common cause of death
causes: CAD, malformation, persistent HTN *(but not from other causes, like cardiac tamponade) |
congestive heart failure (CHF)
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acute or insidious onset
diastolic and/or systolic dysfunction *VENOUS return stays the same or increases. |
pathophysiology of CHF
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– Reflex increased sympathetic activity – how does this occur? baroreceptors
– Release of renin – increases volume and return to heart – mechanism for release? RAA, & stimulate brain thirst centers – Anaerobic metabolism by affected cells – Increased extraction of oxygen from hemoglobin by peripheral cells |
Systemic responses to decreased output from CHF
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-Seen most often in patients with systemic hypertension
-Ventricle undergoes hypertrophy due to increased work load due to increased peripheral resistance -wall enlarges --> chamber volume decreases -->ventricular compliance decreases --> CO declines *ventricular contractilty is normal |
Diastolic dysfunction with CHF
(Ventricle wall thickens) |
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Seen in patients with myocardial damage due to an MI
CO declines but venous return stays the same or increases --> volume of the ventricle increases Hypertrophy of the ventricular wall does NOT occur *Ventricular contractility impaired |
Systolic dysfunction with CHF
Chamber gets huge (enlarged heart) |
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decrease CO --> lowers BP --> renin is released from kidney --> angiotensin --> ACE --> angiotensin II --> stimulates thirst center in brain, causes vasoconstriction, secretion of aldosterone
results: increased BP, expansion of blood volume (via aldosterone) |
Renin-angiotensin-aldosterone system
(RAA) * increases the workload on the already failing heart |
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Right heart failure follows left heart failure
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Right heart failure follows left heart failure
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why does an ANP draw confirm CHF?
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Atrial natriuretic peptide is release from atrial cells when there is increased stretch due to increase blood volume, as in CHF
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-Output of the left ventricle is less than the total volume of blood received from the right side of the heart through the pulmonary circulation
-Pulmonary circuit becomes congested -Systemic blood pressure falls -compensatory mechanisms initiated -Major causes include MI, systemic hypertension, aortic stenosis and insufficiency, cardiomyopathy, mitral stenosis and mitral insufficiency -Blood back into the left atrium due to left ventricular failure -Blood volume in the lungs increases -Above a critical point (25-28 mm Hg), fluid passes across the pulmonary membrane into the interstitial spaces around the alveoli and eventually into the alveoli -Pulmonary edema results when pulmonary lymphatics are unable to handle the additional fluid volume -Recall they can compensate up to 4X the lymph flow -Acute pulmonary edema results as alveoli fill with fluid -Microhemorrhages can occur and sputum may become rust-colored -Hemosiderin-laden macrophages are present – known as heart failure cells -With decreased CO, BP decreased and RAA system stimulated -Sodium and water are retained -Sympathetic neural stimulation increases heart rate and peripheral vasoconstriction -Blood volume increased |
left heart failure
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Output of right ventricle is less than the input from the system venous circuit.
-Systemic venous circuit is congested and output to the lungs decreases -Primary cause of RHF is LHF -Due to excessive pulmonary pressure generated by left heart failure -Other causes include chronic obstructive lung disease, pulmonary embolus, right ventricular infarct, and congenital heart defects -Right heart failure that results from lung disease is called cor pulmonale – common in patients with COPD -Failure of right ventricle to empty causes blood to backup into right atrium, causing increased pressure in the systemic venous circulation -Increased volume and pressure are transmitted to distensible organs such as the liver and spleen -Results in transudation of fluid into abdominal cavity (ascites) and systemic peripheral edema -What is the mechanism for peripheral edema? -Hepatomegaly, splenomegaly, gravity dependent edema results Signs and Symptoms: -Pitting edema noted on sternum or sacrum as well as feet and legs depending on position -Respiratory impingement and organ dysfunction -Deactivation of aldosterone by the liver may lead to additional fluid retention -Jaundice and coagulation problems may result if effects on liver are severe -Jugular venous distension in the neck can be measured at the bedside |
Right Heart Failure
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