The document discusses ventricular dysfunction in critically ill patients. It begins by outlining how left ventricular function is connected to tissue oxygenation through a series of physiological relationships. It then examines the left ventricular pressure-volume relationship and how indices like ESPVR and EDPVR relate to contractility and compliance. Various factors that can cause decreased contractility leading to systolic dysfunction are explored, including reversible acute causes and chronic conditions. Management strategies to address systolic dysfunction like increasing preload, contractility, and decreasing afterload are summarized. The complex interplay between preload and ventricular compliance is also discussed.
2. How much have we deciphered Mother Nature?
“And the LV volume is a surrogate for LV wall tension
And the LV wall tension a surrogate for LV stroke volume
And the LV stroke volume determines CO
And the LV CO is a surrogate for tissue blood flow
And tissue blood flowis a surrogate for tissue oxygenation
And the tissue oxygenation is a surrogate for ATP generation
And ATP generation powers cellular function”
critical care clinic
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5. LV PRESSURE VOLUME CURVE
LVESPVR - index of contractility
150
LV Pressure
100
50
LVESDVR - index of compliance
LV volume
50
130
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6. ESPVR
index of contractility
All ESPV points lie along a line
All ejection from different diastolic volumes end on ESPVR
ESPVR shifts to left when contractility increases
decreased ejection at any given preload and afterload
ESPVR shifts to right when contractility decreases
increased ejection at any given preload and afterload
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7. EDPVR
index of compliance
All EDPV points lie along a line
EDPVR shifts to left and up when ventricular compliance decreases
diastolic dysfunction
EDPVR shifts to right and down when ventricular compliance increases
dilated cardiomyopathy
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11. Decreased Contractility = ventricular systolic dysfunction
Considering normal preload, afterload and ventricular compliance
LVESPVR
150
c-d= stroke volume
130-50= 80
d
d’
50
Isovolemic contraction
c
isovolemic relaxation
LV Pressure
100
a
a’
c-d’= stroke volume
130-80= 50
LVESDVR
b
LV volume
50
80
130
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12. Decreased Contractility = ventricular systolic dysfunction
Increased LVESV: decreased SV and EF
EF or FS dependent on
Preload
Contractility
afterload
Increased LV end systolic volume
with
Normal or decreased afterload
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15. Decreased Contractility = ventricular systolic dysfunction
Causes:
Acute
Respiratory acidosis
causes intracelluar acidosis
Significantly decreases contractility at PaCO2 level of 60
Chronic respiratoryacidosis leads to metabolic compensation
leading to nearly normal intracellular pH
Metabolic acidosis
Less effect as minimal change in intracellular pH
Only metabolic anions permeate cell membrane
Organic anions like lactate, ketoacides do not easliy cross cell membrane
Lactic acidosis begins to depress contractility at pH 7.1 to 7.2
but even at pH 7.0 this depression is quiet small
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16. Decreased Contractility = ventricular systolic dysfunction
Causes:
Acute
Ionized hypocalcemia
Massive PRBC transfusion: citrate bind to Ca
Lactic acid also binds to Ca
Bicarbonate infusion also decreased Ca
Hypokalemia or hyperkalemia
Hypomagnesimia
hypophosphatemia
Bicarbonate infusion
Increases PaCO2: decreases intracellular pH
Increased lactic acid production: by increasing rate limiting step of glycolysis
Decreases ionized Calcium
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17. Decreased Contractility = ventricular systolic dysfunction
Causes:
Acute
Proinflammatory cytokines
TNF ᾳ, IL 1, 2, 6
Increased NO production
Reactive oxygen intermediates
Released by leucocytes
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32. Increasing preload
at normal s.albumin and normal pulmonary capillary permeability
pulmonary starts to develop at Ppaw value of 20-25 mmHg
In critically ill patients s. albumin is decreased and pulmonary capillary permeability
Is increased
Pulmonary oedema will develop at lower Ppaw
Ppaw has many reasons to increase in critically ill patients
Optimal Ppaw has to be identifies which leads to increased stroke volume
With minimal or no pulmonary oedema formation
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33. Increasing preload
In critically ill patients without previous cardiac dysfunction major factor limiting
cardiac output is limited venous return
Limited venous return
Increased venous capacitance: increase unstressed volume
Positive pressure ventilation
Ventricular diastolic dysfunction
Venous return can be increased with
Ionotropes and vasopressors: increase MSFP and decreased resistance to VR
Volume expansion: increasing stressed volume
Benefit and safety margin of vasopressor vs volume expansion has to be evaluated
To avoid ineffective flogging of empty heart
To avoid flooding of lungs and interstitial tissues
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38. Decreased ventricular compliance: diastolic dysfunction
End diastolic volume decreased: decreased SV and EF
EF or FS dependent on
Preload
Contractility
afterload
decreased LV end diastolic volume
with
Normal or increased Pra/ LVEDP
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39. Decreased ventricular compliance: diastolic dysfunction
In the absence of Echocardiography
Should be suspected
when decreased LV pump function is not responding to
fluid expansion/ vasopressors, ionotropic agents and reduction of afterload
Cardiac output is unusually sensitive to changes in heart rate
Late diastolic filling of LV is small in stiff LV
little contribution in EDV by this phase
Increase in HR has less impact on reduction in EDV and therefore SV
Increase in HR, increases C.O. ( CO= SV *HR)
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44. Some facts
right ventricle is thin walled pump, with large radius of curvature
Built for lowpressure system: afterload
Right venricle contraction moves sequentially
from apex to pulmonary outflowtract like peristaltic pump
During diastole RV at normal diastolic pressure lies belowits stressed volume
allowing it to increase preload
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46. RV incrased afterload
Management
•
Management of acute cause
•
Management of ventricular interdependence
Decrease parallel coupling of LV and RV
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47. Some facts to remember
In heart failure, evidence of dependent pulmonary crackles on physical examination,
suggest that LV filling pressure is elevated, usually to more than 20-25mmHg.
However in Chronic heart failure crackles may not be heard even at
Pla more than 30 mmHg as pulmonary lymphatic drainage is increased.
Interstitial odema clearance lags decrease in Pla by hours,
so rapid decrease in Pla is not accuratelyreflected by pulmonary auscultation.
Even before diuresis is established, frusemide reduces Pla by a
venodilatory effect and also reduced intrapulmonary shunt
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48. “The success of intensive care is not,
therefore, to be measured only by the statistics of survival,
as though each death were a medical failure.
It is to be measured by the quality of lives preserved or restored;
and by the quality of the dying of those in whose interest it is to die;
and by the quality of human relationships involved in each death.”
Gordon Dunstan
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