LVP and Ao Flashcards
Normal LVP pressure waveform
systolic, diastolic + end diastolic
Changes with outflow obstruction
Systolic PG → valvular/sub/supra
Normal AoP curve
systolic peak, dicrotic notch, diastolic
types of PG measurements
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
Effect of general anesthesia on PG
General anesthesia ↓ PG 40-50%
What factors can affect PG
Depend on trans valvular flow → affected by HF, anesthetics, hypovolemia, arrhythmia, other lesions ↓ flow
Effect of isoproterenol stim on normal heart
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
Fixed SAS: AoP curve
- Obstruction throughout entire systole: starts at AoV opening → closure
- Aortic pressure: slow rate of rise
o Start early systole → entire ejection period
Fixed SAS: LVP curve
symmetric shape, peak in mid systole
o Largest PG in early systole
Dynamic LVOTO secondary to HCM: AoP curve
rapid upstroke in early systole → flat
o Rapid ventricular ejection → doming due to dynamic obstruction
o Characteristic “spike and dome” → bifid pulse
Dynamic LVOTO secondary to HCM: LVP curve
rapid upstroke is late when maximal obstruction = at end systole
Brockenbrough-Braunwald sign
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
Intermittent obstruction
- 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
Systolic anterior motion of MV
- 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