LVOTO

Question 1

LVOTO (from IBCC notes)

Definition

Answer 1

-> Defined on basis of echocardiography: -
-demonstrable pressure gradient across LVOT ≥ 30 mmHg (commonly >50 mmHg).

*	However, identification of qualitative LVOTO (not precise pressure gradient) may have therapeutic implications.

Question 2

Pathophysiology

Answer 2

• Caused by fast-flowing blood through LVOT which pulls the mitral valve anteriorly towards the outflow tract due to a Venturi effect.
  
  • This anterior motion of MV has consequences:
    1). Obstruction of LVOT → impaired ejection of blood to aorta → ↓ CO → cardiogenic shock
    2). MV not opened during systole → causes MR → ↑ pressure in LA → congestion & APO

Question 3

Causes

Answer 3

=>Anatomical causes
* LVH (esp. base of septum) → narrowed LVOT, high blood velocity & also pushes MV towards LVOT
* MV with large / floppy leaflets

Cardiomyopathies
* Hypertrophic CMP
* Infiltrative CMP (amyloidosis / sarcoid)
* Takotsubo CMP (esp. in classic takotsubo with apical akinesis & hypercontractile base)
* LAD ischemia →with apical hypokinesis

Valvular
* MVRepair (esp. hypermobile ventricle)
* AVR

Question 4

Exacerbating factors

Answer 4

• Tachycardia
• Hypovolaemia(↓ preload)
• Afterload ↓ (e.g. distributive shock, vasodilators)
• Inotropes → ↑ contractility
• Endogenous sympathetic tone
• Diuretics, IABP( all that help MR will worsen LVOTO induced MR)

Question 5

Clinical findings

Answer 5

• Hypotension → obstructive shock (cool peripheries, ⬆️CRT, Tachycardia, Narrow pulse pressure)
• Cardiogenic APO due to MR
• New systolic murmur
• Brisk arterial pulse – rapid rise/run-off
  -** Spike & dome appearance on pressure trace**
• Inotropes → exacerbate shock (positive feedback: ↑ LVOTO → ↓ output → ↑ shock → ↑ vasopressors/inotropes → worse LVOTO)
• May be percieved as vasopressor resistant cardiogenic shock- hence imp. to diagnose LVOTO as a cause of shock.
• **ECG: dagger Q waves (septal hypertrophy)
  
  • Giant T wave in V6 → LVH**

Question 6

Echo findings of LVOTO

Answer 6

1->Ventricle susceptible to LVOTO:
* LVH or small chamber size
* Takotsubo pattern (apical dilation + basal hyperkinesis)
2-> Hyperkinetic LV → near obliteration of LV cavity during systole
3->Mitral Valve
* MR
* SAM: during systole, MV leaflets are sucked towards septum

4->Doppler findings of LVOTO
* Hallmark: high velocity, late-peaking continuous wave Doppler signal from LVOT (described as “dagger-shaped” waveform)
* Late-peaking nature may differentiate it from AS (where rise in velocity is more symmetric)
* LVOT gradient
* 30 mmHg (>2.7 m/s) = pathologically elevated
* 50 mmHg (>3.5 m/s) = severely elevated

Question 7

Management

Answer 7

->Discontinue:
* Inotropes
* Afterload-lowering drugs (e.g., captopril)
* IABP

->Administer
1)* Fluids
2)* Pure vasoconstrictors (preferred as vasopressors of choice)
- Phenylephrine
- Vasopressin
* Vasoconstriction helpful in LVOTO via:
- ↑ Afterload
- ↑ Preload (venoconstriction)
- Reflex bradycardia → improves ventricular filling

3)β-blockers
* Short-acting β-blockers (e.g., Esmolol) may be useful (titrated agent).