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84 Cards in this Set
- Front
- Back
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At what pulse ox sat will you see cyanosis?
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<85%; difficult to see with 88-92%
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Peripheral Cyanosis
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O2 sat may be nl; dt reduced peripheral circ (tissues extract more O2); venous end of caps with reduced Hg; dt cold, polycythemia, acrocyanosis; extremities cold, blue while MM and tongue pink
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Central cyanosis
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dt arterial desaturation, best seen in tongue, MM, trunk.
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Cyanosis of the postductal strucutres (LE and toes), not the preductal structures (fingers) = Differential Cyanosis
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could indicate aortic arch obstruction or persistent pulmonary HTN with ductal R-->L shunting of desaturated blood
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Cyanosis of the preductal structures (fingers) but not the postductal (toes) = Reverse Differential Cyanosis
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indicates TGA, with R-->L shunting of saturated blood through the ductus
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Signs of infective endocarditis on cardiac PE
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petechiae and splinter hemorrhages
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Abnormalities of Arterial Pulses
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Significant radial-fem delay: CoA; rapid rising or bounding pulses: seen with large PDA or aortic valve insufficiency; slow-rising pulses can indicate aortic stenosis or HTN
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Venous Pulses - A wave
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venous wave that occurs just before the first heart sound and is due to atrial contraction. A large A wave usually indicates elevated right ventricular, end-diastolic pressures.
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"Cannon" a waves
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occur when the right atrium contracts against a closed tricuspid valve, which can occur with AV dissociation (3rd degree heart block) or ventricular tachycardia
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Venous Pulses - V wave
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due to increasing volume filling and concomitant, increasing pressure in the right atrium. It begins late in ventricular systole and in diastole; it is large with poor ventricular compliance and in severe TR
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S1 - characteristics
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usually single or narrowly split. NEVER heard better at the base than at the apex. (heard best at apex) Loudness will vary, depending on force of AV valve closure.
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When is S1 loud?
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Mitral Stenosis, increased ventricular contractility, or a short PR interval as the valves come together forcefully at the beginning of systole
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When is S1 soft?
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decreased contractility, as in myocarditis
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Ejection Clicks
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heard near the 1st heart sound and may be difficult to discern initially. Aortic clicks are heard at the apex, pulmonary valve clicks are heard at the base.
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Ejection Clicks with Pulmonary Valve Stenosis
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occur early in systole at the left base of the heart and may vary with respiration
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When do you generally hear systolic ejection clicks?
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when there is an enlarged great vessel at the base of the heart or a thickened, abnormal semilunar valve
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Examples of systolic ejection clicks
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enlarged aorta (Tetrology of Fallot); Trucus Arteriosus; Thrickened semilunar valves (aortic stenosis, bicuspid AV, truncus arteriosus/multi-valved great vessel, pulmonic stenosis)
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When do nonejection clicks occur?
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later in systole and are heard at the LLSB or the apex
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A midsystolic click at the apex suggests…
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mitral valve prolapse
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S2 - characteristics
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reflects closure of the aortic valve, then the pulmonic. Normally physiologic splitting, results from increased venous return with inspiration. (increased RV volume delays RV emptying, delaying closure of pulmonic valve)
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S2 after inspiration
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wide splitting of the second hear sound shortly after inspiration
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What should you think of with perceptible S2 splitting in an infant?
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nomally HR too fast to perceive splitting, thf suspect large L-->R atrial or venous shunt (such as anomolous pulmonary venous return)
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Sounds in TGA
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the aortic valve is anterior and directly under your stethoscope, so aortic closure is very loud and best heard at the ULSB
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Sounds in ToF
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the aorta is wide and dextroposed, and the polmonary artery is located anterior and is smaller than usual; results in a single, S2 loudest at the LLSB
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Aorta positioning is…
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ALP - aorta is leftward and posterior, closes first in split S2
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Persistent Wide Splitting
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is dt delayed RV empyting and can indicate possible ASD, RBBB, or pulmonic stenosis.
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Paradoxically split S2
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splitting during expiration instead of inspiration is due to delay in the LEFT ventricular emptying, with aortic closure AFTER pulmonic. (ie: aortic stenosis, LBBB, and HCM)
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S3 - characteristics
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heard in early diastole, when there is rapid, passive filling of a "relatively stiff" ventricle.
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When is S3 normal?
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Can be nl in children and pregnant women
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When is S3 pathalogic?
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left or right ventricular dysfunction or stiffness and AV valve regurgitation
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S4 - characteristics
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occurs in late diastole, when atrial contraction fillsthe ventricle. ALMOST ALWAYS ABNORMAL.
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When is S4 heard?
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heard with aortic stenosis, mitral regurgitation, HCM, HTN with LV hypertrophy
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Mechanism of "innocent murmurs"
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due to normal slow turbulence and vibration; after age 2, many children with have at least 1 innocent murmur
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MC innocent murmurs of infancy?
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physiological peripheral pulmonic stenosis (PPPS) and occasionally a Still's murmur
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Systolic Innocent Murmurs
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all are short and soft (grade III/VI or less); louder when supine (bc stroke volume increases); louder with exercise, anxiety, anemia, or fever. May get softer or disappear with Valsalva
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Still's Murmur
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SEM with a musical quality or vibratory character, "plucked string instrument or kazoo"; best heard in lower precordium, NOT in the back. Intensity DECREASES with INSPIRATION and positional changes that decrease venous return (ie: standing)
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Basal Ejection Systolic Murmur
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heard at the base; mid-pitched. Difficult to distinguish from mild pulmonic or aortic stenosis or bicuspid AV. STENOSIS usually is HARSHER and LONGER and there may be a systolic EJECTION CLICK (esp on the boards!!)
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Supraclavicular Arterial Bruit
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due to turbulance in the subclavian and carotid arteries, which in turn is due to increased acceleration in early systole. It is very SHORT and EARLY and ends before the 1st third of systole.
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PPPS
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due to fetal anatomy; for several weeks after birth, the R and L pulmonary arteries are much smaller than, and come off at a right angle to, the large main pulmonary artery --> turbulance --> soft, SEM best heard in axillae and both the right and left hemithoraces.
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When should PPPS disappear?
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by 12 months, the branch Pas become larger, and angle opens up
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Venous Hum
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continuous; due to blood draining down the collapsed jugular veins into the dilated intrathoracic veins. The high velocity makes the vein walls "flutter" resulting in a low pitched murmur.
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Maneuvers to make the Venous Hum disappear
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It is usually absent when supine, bc neck veins are distended and pressure gradient b/w 2 areas disappears; also disappears with valsalva maneuver, turning of the head, or compression of the jugular vein
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At what pulse ox sat will you see cyanosis?
|
<85%; difficult to see with 88-92%
|
|
|
Peripheral Cyanosis
|
O2 sat may be nl; dt reduced peripheral circ (tissues extract more O2); venous end of caps with reduced Hg; dt cold, polycythemia, acrocyanosis; extremities cold, blue while MM and tongue pink
|
|
|
Central cyanosis
|
dt arterial desaturation, best seen in tongue, MM, trunk.
|
|
|
Cyanosis of the postductal strucutres (LE and toes), not the preductal structures (fingers) = Differential Cyanosis
|
could indicate aortic arch obstruction or persistent pulmonary HTN with ductal R-->L shunting of desaturated blood
|
|
|
Cyanosis of the preductal structures (fingers) but not the postductal (toes) = Reverse Differential Cyanosis
|
indicates TGA, with R-->L shunting of saturated blood through the ductus
|
|
|
Signs of infective endocarditis on cardiac PE
|
petechiae and splinter hemorrhages
|
|
|
Abnormalities of Arterial Pulses
|
Significant radial-fem delay: CoA; rapid rising or bounding pulses: seen with large PDA or aortic valve insufficiency; slow-rising pulses can indicate aortic stenosis or HTN
|
|
|
Venous Pulses - A wave
|
venous wave that occurs just before the first heart sound and is due to atrial contraction. A large A wave usually indicates elevated right ventricular, end-diastolic pressures.
|
|
|
"Cannon" a waves
|
occur when the right atrium contracts against a closed tricuspid valve, which can occur with AV dissociation (3rd degree heart block) or ventricular tachycardia
|
|
|
Venous Pulses - V wave
|
due to increasing volume filling and concomitant, increasing pressure in the right atrium. It begins late in ventricular systole and in diastole; it is large with poor ventricular compliance and in severe TR
|
|
|
S1 - characteristics
|
usually single or narrowly split. NEVER heard better at the base than at the apex. (heard best at apex) Loudness will vary, depending on force of AV valve closure.
|
|
|
When is S1 loud?
|
Mitral Stenosis, increased ventricular contractility, or a short PR interval as the valves come together forcefully at the beginning of systole
|
|
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When is S1 soft?
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decreased contractility, as in myocarditis
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Ejection Clicks
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heard near the 1st heart sound and may be difficult to discern initially. Aortic clicks are heard at the apex, pulmonary valve clicks are heard at the base.
|
|
|
Ejection Clicks with Pulmonary Valve Stenosis
|
occur early in systole at the left base of the heart and may vary with respiration
|
|
|
When do you generally hear systolic ejection clicks?
|
when there is an enlarged great vessel at the base of the heart or a thickened, abnormal semilunar valve
|
|
|
Examples of systolic ejection clicks
|
enlarged aorta (Tetrology of Fallot); Trucus Arteriosus; Thrickened semilunar valves (aortic stenosis, bicuspid AV, truncus arteriosus/multi-valved great vessel, pulmonic stenosis)
|
|
|
When do nonejection clicks occur?
|
later in systole and are heard at the LLSB or the apex
|
|
|
A midsystolic click at the apex suggests…
|
mitral valve prolapse
|
|
|
S2 - characteristics
|
reflects closure of the aortic valve, then the pulmonic. Normally physiologic splitting, results from increased venous return with inspiration. (increased RV volume delays RV emptying, delaying closure of pulmonic valve)
|
|
|
S2 after inspiration
|
wide splitting of the second hear sound shortly after inspiration
|
|
|
What should you think of with perceptible S2 splitting in an infant?
|
nomally HR too fast to perceive splitting, thf suspect large L-->R atrial or venous shunt (such as anomolous pulmonary venous return)
|
|
|
Sounds in TGA
|
the aortic valve is anterior and directly under your stethoscope, so aortic closure is very loud and best heard at the ULSB
|
|
|
Sounds in ToF
|
the aorta is wide and dextroposed, and the polmonary artery is located anterior and is smaller than usual; results in a single, S2 loudest at the LLSB
|
|
|
Aorta positioning is…
|
ALP - aorta is leftward and posterior, closes first in split S2
|
|
|
Persistent Wide Splitting
|
is dt delayed RV empyting and can indicate possible ASD, RBBB, or pulmonic stenosis.
|
|
|
Paradoxically split S2
|
splitting during expiration instead of inspiration is due to delay in the LEFT ventricular emptying, with aortic closure AFTER pulmonic. (ie: aortic stenosis, LBBB, and HCM)
|
|
|
S3 - characteristics
|
heard in early diastole, when there is rapid, passive filling of a "relatively stiff" ventricle.
|
|
|
When is S3 normal?
|
Can be nl in children and pregnant women
|
|
|
When is S3 pathalogic?
|
left or right ventricular dysfunction or stiffness and AV valve regurgitation
|
|
|
S4 - characteristics
|
occurs in late diastole, when atrial contraction fillsthe ventricle. ALMOST ALWAYS ABNORMAL.
|
|
|
When is S4 heard?
|
heard with aortic stenosis, mitral regurgitation, HCM, HTN with LV hypertrophy
|
|
|
Mechanism of "innocent murmurs"
|
due to normal slow turbulence and vibration; after age 2, many children with have at least 1 innocent murmur
|
|
|
MC innocent murmurs of infancy?
|
physiological peripheral pulmonic stenosis (PPPS) and occasionally a Still's murmur
|
|
|
Systolic Innocent Murmurs
|
all are short and soft (grade III/VI or less); louder when supine (bc stroke volume increases); louder with exercise, anxiety, anemia, or fever. May get softer or disappear with Valsalva
|
|
|
Still's Murmur
|
SEM with a musical quality or vibratory character, "plucked string instrument or kazoo"; best heard in lower precordium, NOT in the back. Intensity DECREASES with INSPIRATION and positional changes that decrease venous return (ie: standing)
|
|
|
Basal Ejection Systolic Murmur
|
heard at the base; mid-pitched. Difficult to distinguish from mild pulmonic or aortic stenosis or bicuspid AV. STENOSIS usually is HARSHER and LONGER and there may be a systolic EJECTION CLICK (esp on the boards!!)
|
|
|
Supraclavicular Arterial Bruit
|
due to turbulance in the subclavian and carotid arteries, which in turn is due to increased acceleration in early systole. It is very SHORT and EARLY and ends before the 1st third of systole.
|
|
|
PPPS
|
due to fetal anatomy; for several weeks after birth, the R and L pulmonary arteries are much smaller than, and come off at a right angle to, the large main pulmonary artery --> turbulance --> soft, SEM best heard in axillae and both the right and left hemithoraces.
|
|
|
When should PPPS disappear?
|
by 12 months, the branch Pas become larger, and angle opens up
|
|
|
Venous Hum
|
continuous; due to blood draining down the collapsed jugular veins into the dilated intrathoracic veins. The high velocity makes the vein walls "flutter" resulting in a low pitched murmur.
|
|
|
Maneuvers to make the Venous Hum disappear
|
It is usually absent when supine, bc neck veins are distended and pressure gradient b/w 2 areas disappears; also disappears with valsalva maneuver, turning of the head, or compression of the jugular vein
|
