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26 Cards in this Set
- Front
- Back
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JVP waves
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a wave: back pressure from RA contraction
C wave: bulge from tricuspid V wave: passive filling X descent: pressure decline following a wave Y descent: tricuspid opens, fall in RA pressure |
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JVP pathologic waves
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Prominent a wave: RV hypertrophy, tricuspid stenosis
Prominent V wave: tricuspid regurgitation Prominent Y wave: constrictive pericarditis |
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JVP measurement
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Is max vertical height above center of RA
Normal is less than 9 cm Calculated at bedside by adding 5 cm to height above sternal angle Be sure to use IJ and not EJ (EJ has valves) |
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Factors in intensity of S1
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Distance separating leaflets at onset of contraction
Mobility of leaflets Rate of ventricular pressure rise |
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Accentuated S1
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PR interval short
-leaflets forced shut from wide distance Mild mitral stenosis -prolonged diastolic pressure gradient keeps mitral leaflets further apart -forced shut loudly Tachycardia -shortened diastole doesn't allow leaflets to drift together -forced shut loudly |
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Diminished S1
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Prolonged PR
-leaflets drift together Mitral regurgitation -leaflets may never come into contact Severe mitral stenosis -leaflets fixed |
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Physiologic splitting
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High frequency, best heard at second left intercostal space next to sternum
S2 heard as one sound during expiration but become audibly separated during inspiration Expansion of chest during inspiration causes intrathoracic pressure to become more negative. Negative pressure transiently increases capacitance of pulmonary vessels There is temporary delay in the diastolic back pressure of the pulmonary artery responsible for the closure of the pulmonic valve Thus P2 is delayed Inspiration has opposite effect on A2 Venous return to LA temporarily decreases Reduced filling of LV diminishes SV and A2 closes earlier |
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Accentuated S2
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Systemic or pulmonary hypertension
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Diminished S2
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Severe aortic or pulmonic valve stenosis
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Widened splitting of S2
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A2 and P2 audibly separated even during expiration and more so during inspiration
Delayed closure of pulmonic valve, occurs during RBBB and pulmonic valve stenosis |
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Fixed splitting of S2
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Widened interval between A2 and P2 that persists unchanged throughout respiratory cycle
Atrial septal defect -chronic right sided volume overload results in high-capacitance, low resistance pulmonary vasculature -Delays back pressure responsible for closure of P2, thus P2 is later |
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Paradoxical splitting of S2
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Separation of A2 and P2 during expiration that fuses into a single sound on inspiration (opposite of normal)
Abnormal delay in closure of aortic valve such that P2 preceeds A2 -LBBB -aortic stenosis |
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Ejection clicks
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Shortly after S1
Sharp, high pitch heard best over aortic and pulmonic areas -early systole Aortic or pulmonic valve stenosis Clicks occuring in mid or late systole are usually the result of systolic prolapse of the mitral or tricuspid valves |
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Opening snap
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Mitral or tricuspid valve stenosis
Sharp, high pitch, timing doesn't change with respiration The more advanced the stenosis, the shorter the A2 to OS interval |
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S3
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Sometimes referred to as ventricular gallop
Early diastole Dull, low pitched Normal in children and young adults -implies supple ventricle In middle aged or older adults, S3 is sign of disease -volume overload |
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S4
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Atrial gallop
Late diastole Dull, low pitched Coincides with contraction of atria Left or right atrium vigorously contracting against a stiffened ventricle Indicates ventricular hypertrophy or myocardial ischemia |
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Summation gallop
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Patient has S1, S2, S3, S4
If heartrate increases S3 and S4 combine to sound like a loud middiastolic low pitched sound |
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Pericardial knock
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High pitched sound
Constrictive pericarditis Later in diastole than OS and louder and earlier than S3 Abrupt cessation of ventricular filling in early diastole -constrictive pericarditis |
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Murmur mechanisms
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Flow across a partial obstruction
Increased flow through normal structure Regurgitant flow Abnormal shunting |
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Murmur shapes
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Crescendo-decrescendo
-rises and then falls off Decrescendo Uniform |
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Systolic murmurs
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Systolic ejection murmur
-aortic or pulmonic valve stenosis Crescendo decrescendo, high frequency, radiates toward neck May be immediately preceded by ejection click Intensity of murmur doesn't correlate well with severity of aortic stenosis -more severe stenosis has later murmur peaks in systole, softened A2 |
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Pansystolic (holosystolic) murmurs
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Regurgitaiton of blood across incompetent mitral, tricuspid valve of VSD
Uniform intensity No gap between S1 and onset Murmur of advanced mitral regurgitation continues through aortic closure -apex, high pitched, blowing, radiates toward left axilla, intensity doesn't change with respiration Murmur of tricuspid valve regurgitaiton -left lower sternal border, radiates to right of sternum, high pitched and blowing, intensity increases with inspiration VSD murmur -4th to 6th L intercostal, high pitched, palpable thrill -smaller the VSD, the greater the turbulence and the louder the murmur |
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Late systolic murmurs
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Mitral regurgitation caused by mitral valve prolapse
Usually preceded by midsystolic click |
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Early diastolic murmurs
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Aortic valve regurgitation
-High pitched Pulmonic regurgitation -pulmonary arterial hypertension -intensity may increase with inspiration |
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Mid-to-late diastolic murmurs
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Stenotic mitral or tricuspid valve
Unique shape -loudest following valve opening, then decrescendos, then intensifies at and of diastole when atrial contraction augments flow Low pitched Can also be caused by hyperdynamic states such as fever, anemia, hyperthyroidism, and exercise Also in advanced mitral regurgitation (along with the expected systolic murmur) due to increased volume of blood |
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Continuous murmurs
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Heard throughout entire cardiac cycle
Persistent pressure gradient Patent ductus arteriosus Sometimes "to-and-fro" murmur from aortic stenosis and regurgitation can be mistaken for continuous murmur |
