This document discusses a case of left ventricular outflow tract (LVOT) obstruction in a septic 60-year-old female patient. LVOT obstruction can occur when there is an anatomical substrate like hypertrophic cardiomyopathy combined with physiological stressors like sepsis that decrease preload and increase contractility. The patient's hypotension worsened due to the LVOT obstruction. Echocardiogram is needed to diagnose and treatment involves increasing preload, decreasing contractility, and using beta-blockers and calcium channel blockers. The importance of recognizing LVOT obstruction in sepsis is discussed as well as prospectively studying the gradient and how it relates to treatment response and mortality.

1. LVOT OBSTRUCTION IN SEPSIS
Dr MANEENDRA
MD, FNB, EDIC

2. CASE VIGNETTE
• 60 yr/f
• DM / HTN / CAD / LVH
• Fever 3 days
• Burning micturition 2 days,
IN ER :
• HR : 130
• BP : 80 / 40
• TEMP : 102F
• Conscious , oriented
• SPO2 : 98% ON RA
FLUID RESUSCITATION – 30 ml/kg
VASOPRESSORS
desaturates and develops crepts
WORSENING HYPOTENSION
LVOTO

3. HCM AND LVOTO
Apical hypertrophy
Symmetrical hypertrophy
Asymmetrical septal hypertrophy without obstruction
Asymmetrical septal hypertrophy with obstruction
Inc LV wall thickness at least 15 mm in one/
more LV myocardial segments
instantaneous peak Doppler LVOT pressure gradient at least
30 mmHg at rest or during physiological provocation

4. PATHOPHYSIOLOGY
HCM,
hypertension
aortic stenosis
mitral valve replacement
or repair
steep aortic
root angle
acute cor
pulmonale
ballooning
syndrome
(Takotsubo)
sigmoid septum
Needs two factors :
• Anatomical substrate and
• Physiological predisposing
conditions

5. PATHOPHYSIOLOGY
Decrease preload Decrease afterload
Increase heart rate Increase contractility
Small and
hypercontractile
LV
Needs two factors :
• Anatomical substrate
• Physiological predisposing
conditions

6. Stress cardiomyopathy –
takatsubocardiomyopathy
hypercontractile LV base
mid and distal akinesia
reduction in LV chamber size
bleeding, diuretics, trauma, or inotrope infusion
crowding at the LV outflow level
results in systolic anterior motion of the mitral apparatus
dynamic obstruction
Hypotension
new prominent systolic ejection
murmur in the left third
parasternal area

7. DIAGNOSIS
• new systolic murmur in the left low sternal border that increases with Valsalva maneuver or
postextrasystole
• Definitive diagnosis requires performing an echocardiogram as soon as possible

8. TREATMENT
Increase preload Increase afterload
Decrease heart rate Decrease contractility
Stop
Diuretics
Vasopressors
Ionotropic agents
Nitrates
Start
IV fluids
B blockers
Ca chnl blockers
Disopyramide

10. ASSESSING CLINICAL IMPROVEMENT

11. IMPORTANCE
IVO occurrence in septic shock patients;
correlation between the intraventricular gradient and volume status and fluid responsiveness;
mortality rate.
prospectively analyzed 218 patients ,septic shock admitted to a general ICU over a 28-month

12. CASE VIGNETTE
• 60 yr/f
• DM / HTN / CAD / LVH
• Fever 3 days
• Burning micturition 2 days,
IN ER :
• HR : 130
• BP : 80 / 40
• TEMP : 102F
• Conscious , oriented
• SPO2 : 98% ON RA
FLUID RESUSCITATION – 30 ml/kg
VASOPRESSORS
desaturates and develops crepts
WORSENING HYPOTENSION
LVOTO

13. Take home message
• Identify existence of a phenomena of LVOT obstruction in ICU
• Learn to measure LVOT pressure gradient using doppler
• Early adequate fluid resuscitation of all sepsis patients
• Use of B blockers once hemodynamics are controlled with vasopressors to reduce the heart rate
• Plan a observational study of measuring LVOT pressure gradient in all septic shock patients and
see how it progresses with treatment and how it influences mortality

14. EYES WILL SEE ONLY WHAT THE MIND KNOWS…….
THANK YOU……