LVP and Ao Flashcards

1
Q

Normal LVP pressure waveform

A

systolic, diastolic + end diastolic

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2
Q

Changes with outflow obstruction

A

Systolic PG → valvular/sub/supra

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3
Q

Normal AoP curve

A

systolic peak, dicrotic notch, diastolic

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4
Q

types of PG measurements

A

instantaneous, peak to peak, mean P difference

 Diastolic PG across AV valve or systolic PG across semilunar v.

o Valve stenosis: ↑ flow from ↑ pressure behind stenosis

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5
Q

Effect of general anesthesia on PG

A

General anesthesia ↓ PG 40-50%

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6
Q

What factors can affect PG

A

Depend on trans valvular flow → affected by HF, anesthetics, hypovolemia, arrhythmia, other lesions ↓ flow

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7
Q

Effect of isoproterenol stim on normal heart

A

β agonist (β1 + β2)
* Base: no LVOT obstruction
* Iso-1: PG = 40mmHg across LVOT
* Iso-2: PG = 65mmHg across LVOT
o ↑contractility → ↑obstruction = dynamic/progressive LVOTO
o Patients w HCM: can have labile LVOTO
o Septal reduction: considered if PG >50mmHg at rest or during provocation/exercise

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8
Q

Fixed SAS: AoP curve

A
  • Obstruction throughout entire systole: starts at AoV opening → closure
  • Aortic pressure: slow rate of rise
    o Start early systole → entire ejection period
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9
Q

Fixed SAS: LVP curve

A

symmetric shape, peak in mid systole
o Largest PG in early systole

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10
Q

Dynamic LVOTO secondary to HCM: AoP curve

A

rapid upstroke in early systole → flat
o Rapid ventricular ejection → doming due to dynamic obstruction
o Characteristic “spike and dome” → bifid pulse

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11
Q

Dynamic LVOTO secondary to HCM: LVP curve

A

rapid upstroke is late when maximal obstruction = at end systole

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12
Q

Brockenbrough-Braunwald sign

A

o Narrowing pulse pressure w spike/dome appearance after Valsalva/VPC
o After compensatory pause from VPC → drop in Ao pulse
 Fixed obstruction: ↑ contractile force post VPC beat → ↑LV + AoP → ↑CO → ↑pulse width
 Dynamic obstruction: ↑ contractile force worsen → ↑ degree of obstruction → ↑LVP but ↓AoP → ↓ pulse pressure

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13
Q

Intermittent obstruction

A
  • Obstructions can be intermittent
    o Minimal or no PG at rest
    o Provocative maneuvers can be considered to provoke PG
     ↓pre/afterload: nitrates
     ↑contractility: isoproterenol
  • Excessive inotropic stimulation may provoke gradients in normal hearts
     Induce VPC w KT in RV/LV
     Valsalva maneuver: ↑ intrathoracic P → ↓ preload → ↑ obstruction
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14
Q

Systolic anterior motion of MV

A
  • Acceleration of blood flow across LVOT in systole → push MV leaflets in LVOT
  • Dynamic component → peak PG is delayed until late systole
    o LV pressure contour ↑ in late systole
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