Ventricular Dysfunction in Critically Ill

Ventricular dysfunction in
Critically Ill
Uoaur Ranaman
Snr RsnI, CrIcaI Car
Lcn
S.G.F.G./.L.S.
Lucknw, /na
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
How much have we deciphered Mother Nature?
And tissue blood flow is a surrogate for tissue oxygenation
And the tissue oxygenation is a surrogate for ATP generation
And ATP generation powers cellular function
critical care clinic
UauI Ranaman, SnI RsnI, CIIcaI CaI Mcn,
S.G.F.G./.M.S., LucKnw, /na
Ventricular function
PRELOAD
AFTERLOAD CONTRACTILITY
DIASTOLIC
COMPLIANCE
PRELOAD
VALVE
FUNCTION
HEART RATE
VENTRICULAR
PRESSURE- VOLUME PRESSURE- VOLUME
RELATIONSHIP
LVESPVR
100
150
L
V

P
r
e
s
s
u
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e
LV PRESSURE VOLUME CURVE
- index of contractility
LV volume
50
130
50
LVESDVR
L
V

P
r
e
s
s
u
r
e
- index of compliance
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 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
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
c
d
LVESPVR
100
150
L
V

P
r
e
s
s
u
r
e
LV PRESSURE VOLUME CURVE
a-MV opens
b-MV closes
c-AV opens
d-AV closes
a-b = preload
b-c = afterload
LV volume
a
b
50
130
50
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LVESDVR
L
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P
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b-c = afterload
c-d = stroke volume
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End systolic length
CARDIAC MUSLCE LENGTH TENSION CURVE
Muscle length
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End diastolic length
Decreased ventricular contractility Decreased ventricular contractility
systolic dysfunction
c
d
LVESPVR
100
150
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Decreased Contractility = ventricular systolic dysfunction
Considering normal preload, afterload and ventricular compliance
c-d= stroke volume
130-80= 50
d
c-d= stroke volume
130-50= 80
LV volume
a
b
50
130
50
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LVESDVR
L
V

P
r
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s
s
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e
130-80= 50
80
a
EF or FS dependent on
Preload
Contractility
afterload
Increased LVESV: decreased SV and EF
Increased LV end systolic volume
with
Normal or decreased afterload
afterload
c
LVESPVR
100
150
L
V

P
r
e
s
s
u
r
e
Compensatory response of Nature
c-d= stroke volume
130-80= 50
d
Increased SVR
Increased MSFP
Increased VR
Increased LVEDV
Increased HR
c
LV volume
a
b
50
130
50
LVESDVR
L
V

P
r
e
s
s
u
r
e
80
c-d= stroke volume
150-80= 70
150
b
Increased O2 cost
Pulmonary oedema
Myocardial ischemia
Causes:
Acute
Myocardial Intracelluar Acidosis
Decreased affinity of Calcium to contractile proteins
Causes:
Acute
Respiratory acidosis
causes intracelluar acidosis
Significantly decreases contractility at PaCO2 level of 60
Chronic respiratory acidosis 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
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
Causes:
Acute
Proinflammatory cytokines
TNF , IL 1, 2, 6
Increased NO production
Reactive oxygen intermediates
Released by leucocytes
Causes:
Chronic
Idiopathic
Coronary artery disease
Inflammatory: viral, toxoplasmosis, chagas disease
Alcoholic Alcoholic
Infective: HIV
Postpartum
Uremic
Diabetic
Nutritional deficiency: selenium deficiency
Metabolic disorders: fabry disease, Gaucher disease
Toxic: Adriamycin, cobalt
Management
Correcting acute reversible causes
Ishemia
Acidosis Acidosis
Dyselectrolytemia
hypothermia
Management
Increasing
PRELOAD
Decreasing
AFTERLOAD
Increasing
CONTRACTILITY
PRELOAD
Increasing preload
increasing MSFP: increasing Stress volume
Increased venous tone by sympathetic nervous system
Fluid retention by kidneys
Volume optimization
C
a
r
d
i
a
c

o
u
t
p
u
t
6
8
10
12
Guytonian Cardiac function Curve
Increasing preload
increasing MSFP
Pra
C
a
r
d
i
a
c

o
u
t
p
u
t
-5 0 5 10 15 20
2
4
6
25
c
LVESPVR
100
150
L
V

P
r
e
s
s
u
r
e
Increasing preload
increasing MSFP
c-d= stroke volume
160-80= 80
d
c-d= stroke volume
130-80= 50
c
LV volume
b
50 130
50
LVESDVR
L
V

P
r
e
s
s
u
r
e
160-80= 80
80
a
b
160
Increasing preload
increasing MSFP
Fluid
crystalloid vs colloid
Safety margin: interstitial oedema
Can be increased by
Safety margin: interstitial oedema
vasopressures
Increasing preload
increasing ventricular compliance
Increasing EDV without further increase in EDP
Stress relaxation of pericardium and myocardium
Usual response in dilated cardiomyopathies
In septic shock patients,
response of surviving patients is increasing ventricular diastolic compliance
Heart in sepsis, Textbook of Critical Care Medicine, Shoemaker
c
LVESPVR
100
150
L
V

P
r
e
s
s
u
r
e
Increasing preload
increasing ventricular compliance
c-d= stroke volume
160-80= 80
d
c-d= stroke volume
130-80= 50
c
LV volume
b
50 130
50
LVESDVR
L
V

P
r
e
s
s
u
r
e
160-80= 80
80
a
b
160
LVESDVR
Increasing preload
increasing ventricular compliance: double edged sword
parietal pericardium has high extensibility at low level of stretch
with an abrupt transition to relative inextensibility at higher stretch.
Pericardium acts as limiting membrane, restricting cardiac filling at high intracardiac volume
Therfore decreasing ventricular compliance: diastolic dysfunction
Pericardium acts as limiting membrane, restricting cardiac filling at high intracardiac volume
Pericardial P- V curve of dead canine
heart
Ppc vs intracardiac volume
Pericardial disease, P.S. Reddy, Donald F.Leon, James A.Shaver, Raven Press
Intracardiac
Pericardial P- V curve of isolated dog heart
Role of pericardium
Intact pericardium
----Intrapericardial volume
Intracardiac volume
Pericardium removed
( intracardiac volume)
Pericardial disease, P.S. Reddy, Donald F.Leon, James A.Shaver, Raven Press
Increasing preload
increase Pra = increase Ppc = Pulmonary odema
Ponc = 21 21 21 21 21
Ppc = 15 13 11 9 7
Ppc-Ponc = -6 -8 -10 -12 -14
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
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
c
d
LVESPVR
100
150
L
V

P
r
e
s
s
u
r
e
Increasing contractility
c-d= stroke volume
130-80= 50
d
c-d= stroke volume
130-50= 80
LV volume
a
b
50
130
50
LVESDVR
L
V

P
r
e
s
s
u
r
e
80
130-50= 80
a
c
LVESPVR
100
150
L
V

P
r
e
s
s
u
r
e
Decreasing afterload
c-d= stroke volume
130-80= 50
d
c-d= stroke volume
130-55= 75
d
c
LV volume
a
b
50
130
50
LVESDVR
L
V

P
r
e
s
s
u
r
e
80
130-55= 75
55
a
c
Decreased ventricular compliance Decreased ventricular compliance
diastolic dysfunction
c
d
LVESPVR
100
150
L
V

P
r
e
s
s
u
r
e
Decreased ventricular compliance: diastolic dysfunction
c c-d= stroke volume
100-50= 50
c-d= stroke volume
130-50= 80
LV volume
a
b
50 130
50
LVESDVR
L
V

P
r
e
s
s
u
r
e
b
100-50= 50
100
LVESDVR
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
afterload
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)
Myocardial ischemia
delayed systolic relaxation leading to stiffness
Diastolic stiffness precedes depressed contractility
Causes:
Acute
Increased intrathoracic pressure Increased intrathoracic pressure
Increased intrapericardial pressure
positive pressure ventilation, pneumothorax, massive pleural effusion
Increased intraperitoneal pressure
Catecholemines and calcium infusion
hypothermia
Concentric ventricular hypertrophy
HOCM
Causes:
Chronic
Restrictive CMP
Constrictive pericarditis
Identify Optimal filling pressures
that maximizes LVEDV without causing substantial pulmonary odema
Treatment of causes
Ischemia, pneumothorax
Increased pleural, pericardial, abdominal pressures
Optimized intrathoracic pressure in PPV patients: low tidal ventilation strategy
Management:
Optimizes volume status
correct hypovolemia aggressively and promptly not overlooking safety margin
Optimize Ionotropes and vasopressor doses
smallest dose that achieves desired systolic and vascular effect
Tachycardia, arrhythmias should be treated early
Hypothermia should be avoided
The The
Right Ventricle
right ventricle is thin walled pump, with large radius of curvature
Built for low pressure system: afterload
Right venricle contraction moves sequentially
from apex to pulmonary outflow tract like peristaltic pump
Some facts
During diastole RV at normal diastolic pressure lies below its stressed volume
allowing it to increase preload
Pulmonary embolism
Hypoxic pulmonary vasoconstriction
Acidemic pulmonary vasoconstriction
ARDS
Sepsis
RV incrased afterload
acute
Chronic hypoventilation
Recurrent pulmonary embolism
PPH
Chronically elevated LA pressure: MS, LVF
Chronic
Management of ventricular interdependence
Management of acute cause
RV incrased afterload
Management
Management of ventricular interdependence
Decrease parallel coupling of LV and RV
However in Chronic heart failure crackles may not be heard even at
Pla more than 30 mmHg as pulmonary lymphatic drainage is increased.
In heart failure, evidence of dependent pulmonary crackles on physical examination,
suggest that LV filling pressure is elevated, usually to more than 20-25mmHg.
Some facts to remember
Interstitial odema clearance lags decrease in Pla by hours,
so rapid decrease in Pla is not accurately reflected by pulmonary auscultation.
Even before diuresis is established, frusemide reduces Pla by a
venodilatory effect and also reduced intrapulmonary shunt
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
THANK YOU THANK YOU

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