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ECOS III Fall > Dr. Tyler Heart Sound lecture > Flashcards

Dr. Tyler Heart Sound lecture Flashcards

1
Q

Aortic stenosis etiology presentation and heart sound?

A
  • Age releated calcific degeneration or Rheumatic disease
  • Presents with angina syncope and HF, diminished carotid upstroke, weak pulse in later or severe AS
  • Harsh crescendo decrescendo systolic murmur
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2
Q

Where is aortic stenosis heard best?

A

Second right intercostal with radiation to carotid

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3
Q

Aortic regurgitation etiology and clinical presentation?

A
  • aortic root problems due to
    • age
    • htm
    • ankylosing spondylitis
    • syphilis
    • dissection
    • marfans
  • Dyspnea, PND, orthopnea, palpitations laying down, wide pulse pressure bounding pulse
  • Diastolic blowing decrescecndo murmur heard at left sternal border/ apex
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4
Q

Mitral Stenosis etiology and clinical presentation?

A
  • Rheumatic fever mitral annular calcification or congenital
  • Dyspnea hemoptysis, A fib
  • Opening snap, low pitched diastolic rumble and loud S1
    • Best hear when patient left latral decubitis
      Rheumatic fever, mitral annular calcification (e.g.,
      in the setting of CKD), congenital
      Clinical presentation:
      •Dyspnea, hemoptysis, Afib, risk of emboli.
      •Dilated LA can compress the recurrent laryngeal
      nerve and cause hoarseness (severe cases)
      Heart sound:
      •Opening snap, low-pitched diastolic rumble, and
      loud S1
      •Best heard at the apex when the patient is in the
      left lateral decubitus position
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5
Q

What heart murmur has hoarseness associated with it?

A

Mitral stenosis due to dilated LA compressing recurrent laryngeal nerve

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6
Q

Mitral regurgitation etiology and presentation?
Rheumatic fever, mitral annular calcification (e.g.,

A
  • Acute: endocarditis, MI with papillary muslce rupture and chordae tendinae
  • Chronic: valve issue or secondary to dilation of MV annulus (dilated cardiomyopathy)
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7
Q

MR presentation?

A
  • acute pulmonary edema shock and death
  • chronically PE and RF
  • Holocystolici murmur heard at apex radiating to axilla back or clavicle
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8
Q

TR Etiology and presentation?

A
  • Primary valve issue or seondary to RV pressures
  • murmur like MR, holocsystolic, but louder with inspiration
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9
Q

Late cyanosis with L to R?

A
  • ASD
  • PFO
  • VSD
  • PDA
  • CoA
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10
Q

What causes ASD and presentation?

A
  • defect in ostum secundum or ostum primum (in downsyndrome)
  • asx if small, large closed and found in childhood
    • if not closed, dyspnea, exercise intolerance, fatigue
  • Loud S1, wide fixed split S2
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11
Q

Complications of ASD?

A

Pulmonary htn, eisenmenger syndrome, right HF, A fib, stroke with paradoxical emboli

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12
Q

In a patient under 60 with a stroke what cause needs to be considered?

A

PFO

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13
Q

VSD causes, associattions, presentations?

A
  • defect in muscular or membranous portion of ventricular septum
  • FAS and Down syndrome
  • Large VSD deteced and closed, if not patients become symptomatic with pulmonary htn and r to l shunting
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14
Q

VSD sound?

A

harsh blowing holosystolic murmur with thrill loudest at left third intercostal space with hand grip

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15
Q

PFO sound

A
  • Loud S1
  • Wide fixerd split S2
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16
Q

TR sound

A

holosystolic but louder with inspiration

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17
Q

MR sound

A

Holosystolic

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18
Q

MS sound?

A
  • Opening snap and low piptched diastolic rumble
  • loud s1
  • heard best at apex and left lateral decubitus position
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19
Q

PDA etiology and presentation?

A
  • persistent communication btw aorta and pulm artery associated with rubella and prematurity
  • Small asx
  • moderate eisenmenger syndronme
  • Large infantile HF
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20
Q

PDA sound

A

Machine like murmur heard best at the left second intercostal space, wide pulse pressure and bounding peripheral pulses

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21
Q

Eisenmenger syndrome?

A
  • Cyanosis, fatigue, R HF in kids
  • Adults:
    • cyanosis clubbing RV pulse, narrow split S2, absent VSD murmur
    • J VD
  • PDA becomes R to L shunt delivering unoxygenated blood
22
Q

Pulm htn signs>

A
  • Syncope
  • Atrial and vent arrhythmia
  • Cyanosis
  • R and L HF
23
Q

Infantile Coarctation of Aorta?

A
  • LE cyanosis with weak pulses assoc with turners
24
Q

Adult CoA?

A
  • UE htn and low LE BP diminished femoral pulse
  • CSR shows notched ribs due to erosion by collateral arteries
25
Q

Inspiration: lounder ____side heart murmur

A

Right

26
Q

Expiration: louder _ side heart murmur

A

L

27
Q

Standing/Valsalva increases what murmurs?

A
  • MVP
  • HCM
28
Q

Hand grip increases _________ murmurs

A
  • AR
  • MR
  • VSD
29
Q

Hand grip decreases ______ murmurs?

A

HCM

30
Q

Systolic Murmurs

A
  • AS
  • MR
  • TR
  • VSD
  • ASD
  • HCM
31
Q

diastolic murmurs

A
  • AR
  • MS
  • TS
32
Q

What are the major determinants of A2 intensity

A
  • aortic pressure
  • relative proximity of aorta to chest wall
  • size of root
  • mobility and integrity of valve
33
Q

Intensity of P2 is determined by?

A
  • Pulm art pressure
  • size of pulm art
  • Mobiltihy and integrity of valve
34
Q

What is associated with an increased A2 intensity/

A
  • Systemic htn
  • CoA
  • Ascending aortic aneurysm
  • Aortic root being anterior and closer to ant chest wall like in tetraoloy of fallot and transpositon
35
Q

What is assoc with incrweased intensity of P2

A
  • pulm htn
  • idiopatic pulm art dilation
  • ASD
  • Increased with MR (A2 is soft)
36
Q

Decreased intensity of A2?

A
  • conditions that affect mobility and integrity of aortic valve
  • severe AR or stenosis
  • Hypotensison
37
Q

Decreased P2

A
  • Conditiosn that affect mobility and integrity of pulm valve
  • pulm stenosis and regurg
  • Significant RV outflow obsruction assoc wit hsoft and delayed P2
38
Q

Mechanisms for splitting S2

A
  • Has to do with longer RV ejection during inspiration compared with the LV which is correlated with increased right sided and decreased left sided filling
39
Q

What causes wide splitting of S2

A
  • Electromechanical delay of RV such as RBBBB and WPW, also rpemature beats
  • Hemodynamic causes such as resistancce RV ejection and reduction in LV ejection
40
Q

Fixed S2 split causes?

A
  • ASD!!
  • also RV failure
  • RV outflow ibstruction
  • Pulm htn
  • Primary RV dystunction
41
Q

Reversed Paradoxical Splitting of S2?

A
  • Electromechanical delay
    • Left bundle branch block, artificial RV pacing, preexcitation of the RV (WPW syndrome), and premature beats of RV origin are examples of conduction disturbances associated with delayed activation of the LV, and consequently delayed completion of LV ejection causes a delayed A2 and reversed splitting of S2.
  • Hemodynamic
    • •A markedly prolonged LV ejection time may delay A2 sufficiently to cause reversed splitting of S2. With fixed LV outflow tract obstruction, as in patients with aortic valve stenosis, LV ejection time is lengthened, and reversed splitting of S2 usually indicates hemodynamically significant outflow obstruction.•A prolonged LV ejection time and reversed splitting of S2 can occur with myocardial dysfunction, as in myocardial ischemia, or in patients with long-standing severe AR
42
Q

S3?

A

ventricular gallop, early diastolic sound from turbulent flow of blood hitting overfilled ventricle, specific sign of decompensatied heart failure, normal in pregnancy and those <35 yo

43
Q

S4?

A
  • Stiff ventricle, late diastolic, always pathologic in those >40, may be common in athletes
  • Assoc with Vent hypertrophy secondary to Htn, HF
44
Q

Patient > 60 years of age presents with gradual onset:

  • •Decreased exercise tolerance because of fatigue
  • •Exertional dyspnea•
  • Weak carotid pulse with slow rate of rise•
  • Harsh, crescendo-decrescendo, systolic murmur, loudest at the RUSB → neck
  • •Absent S2 split

What is this?

A

aortic stenosis

•Remember that the loudness and the timing of the murmur correlate with severity: Louder, later murmurs (closer to S2) mean more severe disease.•”Pulsus parvus et tardus” is the phrase used to describe the pulse finding in severe AS, where the pulse is generally diminished (weak) with a slow rise (delayed).•As disease worsens, patients may develop syncope, angina, and heart failure.

45
Q

Patient with h/o bicuspid aortic valve presents with:

•Dyspnea on exertion• Î SBP, ￬ DBP, and “water-hammer pulse”•High-pitched, blowing, diastolic murmur (louder with squat and handgrip, softer with Valsalva) loudest at left midsternal border while leaning forward with held expiration•Early systole peaking ejection also audible at the LLSB and apex± Diastolic rumbling, loudest at the apex

A
  • chronic AR
  • •The associations to make with chronic AR are bicuspid valve and Marfan’s (rare).•An increased SBP with a low DBP is termed a “wide pulse pressure.” You’re unlikely to see the words “wide pulse pressure” in a question but note the wide difference between the systolic and diastolic pressures.
  • •“Water-hammer pulse” refers to a brisk fill with a sudden collapse and is sometimes called a Corrigan pulse.•In severe AR, the clinical scenario could include symptoms and signs of LV failure
  • .•Know that acute AR presents differently, and that acute endocarditis is more often suspected in patients with acute AR. Acute AR is a medical emergency with the patient presenting as very sick!
46
Q

Pregnant patient with no PMH presents with 1 week of:

•Exertional dyspnea•Paroxysmal nocturnal dyspnea•Cough with foamy hemoptysis•Nl to ↑JVP•Loud S1 and loud P2 component of S2 split•Diastolic snap sound, audible at apex•Low-pitched, diastolic rumble after the snap, heard only at the apex in left lateral decubitus position

A
  • •Note that the S1 and P2 component of S2 is accentuated in MS; the diastolic murmur crescendos into the S1 sound, making S1 quite loud.
  • •The diastolic snap of MS is best heard at the apex, in the mitral area.
  • •In pregnancy, the MS murmur is often very difficult to hear, so a clinical case might leave the murmur out of the scenario. Be suspicious of MS in any pregnant patient who develops acute pulmonary symptoms with foamy hemoptysis.•Increased cardiac output in pregnancy often results in presentation of previously unknown MS.
  • •CXR shows a triad of (a) prominent pulmonary artery vascularity, (b) an enlarged left atrium, and (c) normal-sized left ventricle.
47
Q

Patient with h/o (Coronary Heart Disease (CHD) presents with gradual:

•Orthopnea•Dyspnea on exertion•Decreased exercise tolerance•Fatigue•Hyperdynamic precordium, displaced to the left•Holosystolic murmur, loudest over the apex, with radiation to the axilla; murmur increases with handgrip±S3

A

Mitral Regurgitation (chronic)

•The holosystolic MR murmur often obscures both S1 and S2

.•An S3 is sometimes present, with the murmur + S3 sounds mimicking “wow-duh.”

  • Know that if the MR is due, in part, to mitral valve prolapse, the clinical scenario could include a midsystolic click that precedes the mitral murmur. If the patient has LV systolic dysfunction, the case could include SSxs of biventricular failure and pulmonary HTN.
  • Any patient with pulmonary HTN, regardless of cause, has a widely split S2 with an increased P2 sound.
48
Q

Patient with a history of severe COPD presents with:

•Increased work of breathing•Pursed-lip breathing•Grade III/VI systolic murmur at the left lower sternal border•Murmur increases with inspiration

A
  • •Chronic TR is often a functional result of RV (right ventricular) dilation, which can be caused by end-stage left ventricular failure, pulmonary embolism, pacemaker/implantable cardioverter-defibrillator leads (which prevent coaptation of tricuspid leaflets), or other causes of pulmonary hypertension as in this script of a patient with severe COPD experiencing an acute exacerbation
  • .•Chronic TR can also be caused by rheumatic heart disease, endocarditis, carcinoid, and congenital disease (Ebstein anomaly)
  • .•Endocarditis affecting the tricuspid valve is typically seen in IV drug abusers, and it is often caused by Staphylococcus; also consider Candida.
49
Q

What murmurs are louder with squatting and expiration?

A
  • AS
  • Chronic AR
  • Acute AR
  • MS
  • Acute MR
50
Q

What murmurs are louder with handgrio?

A
  • ASD
  • CoA

(handgrip decreases HOCM and PDA)

ECOS III Fall (2 decks)

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