Question 11

College answer

Aim: To explore the issues in cardiac anatomy leading to haemodynamic instability with a particular focus on post cardiac surgery in part c.
Key sources include: Related question regarding dynamic left ventricular outflow tract obstruction in paper 2019.1 Q8. CanMEDS Medical Expert.
Discussion: Some candidates did very well, demonstrating an in-depth knowledge of the pathophysiology of SAM and dynamic LV outflow tract obstruction.
Understanding the pathophysiology is key to outlining the specific management. Expert pass answers outlined specific management of the unstable post cardiac surgery patient in detail and showed an understanding of the pathophysiology. These approaches gained more marks than answers which were superficial and contained generic statements. Examples of the expert pass specific management answers included the following:

• Outlining methods of rate control and its subsequent effect on reducing or worsening LVOT obstruction.
• A potential requirement for return to theatre in the post operative valve replacement (most common in the post operative AVR) demonstrating an understanding of the mechanics of obstructive shock in this context and requirement for definite treatment.

Discussion

Question 8 from the first paper of 2019 asked mostly about LVOT obstruction in a generic sense, where SAM was only one of the possible causes.

a)

SAM is the displacement of the distal portion of the anterior leaflet of the mitral valve toward the left ventricular outflow tract. 

This was a 20% SAQ fragment, and so probably more than just this brief definition was expected. One could expand on it by including some echocardiographic criteria:

• Grade 1 – AML buckling towards LVOT 10 mm away from septum
• Grade 2 - AML buckling towards LVOT within 10 mm  from septum
• Grade 3 - AML buckling and touching septum but less than 30% of systole
• Grade 4 - AML buckling and touching septum but more than 30% of systole

Additionally, severity can be assessed by measuring the pressure gradient along the LVOT, where moderate SAM has a maximum pressure gradient of 20 -50 mmHg,  and severe is higher.

b)

Risk factors include:

• Redundant anterior leaflet
• Redundant posterior leaflet
• Papillary muscle displacement 
• Asymmetric septal hypertrophy
• Anatomical anomaly of the chordae
• Small LV chamber volume (for example, due to hypovolemia)
• Increased LV contractility (for example, due to stress or inotropes)
• Undersized mitral annulus
• Anterior displacement of the mitral valve (congenitally, surgically or by disease)
• Low anterior-posterior length ratio of the valve (i.e. ovoid valve)

c)

Specific management of LVOT obstruction in general also covers the management of SAM, and would be something like this:

• Preload: keep it high-normal. 
• Rate: keep it slow. 
• Rhythm: keep it sinus. 
• Contractility: bring it down. Negative inotropes are often called for, eg. beta-blockers
• Afterload: keep it high. Use vasopressors with minimal beta effect (eg. vasopressin or phenylephrine)
• Fix the valve or open out the outflow tract: the patient may need to return to theatre.
• Reduce stressors that would ordinarily increase cardiac contractility: this means, for example, not extubating the patient while waiting for SAM-corrective surgery, and using generous analgesia.