Ventricular dysfunction in_critically_ill

Ventricular dysfunction in
Critically Ill
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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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Ventricular function
DIASTOLIC
COMPLIANCE

PRELOAD

HEART RATE

CONTRACTILITY

AFTERLOAD

VALVE
FUNCTION


VENTRICULAR
PRESSURE- VOLUME
RELATIONSHIP


LV PRESSURE VOLUME CURVE

LVESPVR - index of contractility

150

LV Pressure

100

50

LVESDVR - index of compliance
LV volume
50

130


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


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


LV PRESSURE VOLUME CURVE
a-MV opens
b-MV closes
c-AV opens
d-AV closes

LVESPVR

150

100

d
Isovolemic contraction

50

isovolemic relaxation

LV Pressure

c

a

a-b = preload
b-c = afterload
c-d = stroke volume

LVESDVR

b
LV volume

50

130


CARDIAC MUSLCE LENGTH TENSION CURVE

Isometric contraction

Isometric relaxation

Muscle tension

End systolic length

End diastolic length

Muscle length


Decreased ventricular contractility
systolic dysfunction


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



Increased LVESV: decreased SV and EF

EF or FS dependent on
Preload
Contractility
afterload

Increased LV end systolic volume
with
Normal or decreased afterload


Compensatoryresponse of Nature
130-80= 50
LVESPVR
150

d’

100
LV Pressure

Increased SVR
Increased MSFP
Increased VR
Increased LVEDV
Increased HR

c

c’
c’-d’= stroke volume
150-80= 70

50

a’

b

b’

LVESDVR

Increased O2 cost
Pulmonary oedema

LV volume
50

80

130 150



Causes:
Acute
Myocardial ischemia

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 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


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 ᾳ, IL 1, 2, 6
Increased NO production

Reactive oxygen intermediates
Released by leucocytes



Causes:
Chronic
Idiopathic
Coronary arterydisease
Inflammatory: viral, toxoplasmosis, chagas disease
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
Dyselectrolytemia
hypothermia


Management

Increasing
PRELOAD

Increasing
CONTRACTILITY

Decreasing
AFTERLOAD


Increasing preload
increasing MSFP: increasing Stress volume

Increased venous tone by sympathetic nervous system
Fluid retention by kidneys

Volume optimization


Increasing preload
increasing MSFP
12

Guytonian Cardiac function Curve
10

Cardiac output

8

6

4

2

-5

0

5

10

15

20

25


Pra

Increasing preload
increasing MSFP

LVESPVR
150

c-d= stroke volume
130-80= 50

d’

LV Pressure

100

c

c’

160-80= 80

50

b’ LVESDVR
a’

b
LV volume

50

80

130

160


Increasing preload
increasing MSFP
Can be increased by

Fluid
crystalloid vs colloid
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

Increasing preload
increasing ventricular compliance

LVESPVR
150

c-d= stroke volume
130-80= 50

d’

LV Pressure

100

c

c’

160-80= 80

50
LVESDVR

a’

b

LVESDVR’

b’
LV volume

50

80

130

160


Increasing preload
increasing ventricular compliance: double edged sword

parietal pericardium has high extensibility at lowlevel 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


Pericardial P- V curve of dead canine
heart
Ppc vs intracardiac volume

Intracardiac

Pericardial disease, P.S. Reddy Donald F.Leon, James A.Shaver, Raven Press
,


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


Increasing contractility

LVESPVR
150

130-80= 50

LV Pressure

100

d’’

d’
c-d= stroke volume
130-50= 80

c

50
LVESDVR

b

a’’

a’
LV volume

50

80

130


Decreasing afterload

LVESPVR
150

130-80= 50

LV Pressure

100

d’’

d’
c
c’

c-d’’= stroke volume
130-55= 75

50
LVESDVR

a’

a’’

b
LV volume

55

50

80

130


Decreased ventricular compliance
diastolic dysfunction


Decreased ventricular compliance: diastolic dysfunction

LVESPVR

150

c-d= stroke volume
130-50= 80

LV Pressure

100

d
c’

c’-d= stroke volume
100-50= 50

c

LVESDVR’
50

b’
a

LVESDVR

b
LV volume

50

100 130



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



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)

Causes:
Acute
Myocardial ischemia
delayed systolic relaxation leading to stiffness
Diastolic stiffness precedes depressed contractility

Increased intrathoracic pressure
Increased intrapericardial pressure
positive pressure ventilation, pneumothorax, massive pleural effusion
Increased intraperitoneal pressure

Catecholemines and calcium infusion
hypothermia


Causes:

Chronic

Concentric ventricular hypertrophy
HOCM
Restrictive CMP
Constrictive pericarditis


Management:
Treatment of causes
Ischemia, pneumothorax
Increased pleural, pericardial, abdominal pressures
Optimized intrathoracic pressure in PPV patients: lowtidal ventilation strategy
Identify Optimal filling pressures
that maximizes LVEDV without causing substantial pulmonary odema
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
Right Ventricle


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


RV incrased afterload
acute
•
Pulmonaryembolism
•
Hypoxic pulmonary vasoconstriction
•
Acidemic pulmonary vasoconstriction
•
ARDS
•
Sepsis
•
Positive pressure ventilation

Chronic
•
Chronic hypoventilation
•
Recurrent pulmonary embolism
•
PPH
•
Chronically elevated LA pressure: MS, LVF


RV incrased afterload
Management

•
Management of acute cause

•
Management of ventricular interdependence
Decrease parallel coupling of LV and RV


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


“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


Ventricular dysfunction in_critically_ill

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