Ventricular dysfunction in_critically_ill

Ventricular dysfunction inCritically Ill

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“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

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Ventricular function

PRELOAD AFTERLOADCONTRACTILITY

DIASTOLIC COMPLIANCE

PRELOAD AFTERLOADCONTRACTILITY

VALVE FUNCTION

HEART RATE

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VENTRICULARPRESSURE- VOLUMEPRESSURE- VOLUME

RELATIONSHIP

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LVESPVR

100

150

LV P

ressure

LV PRESSURE VOLUME CURVE

- index of contractility

LV volume

50 130

50

LVESDVR

LV P

ressure

- index of compliance

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ESPVRindex of contractility

All ESPV points lie along a line

All ejection from different diastolic volumes end on ESPVR

ESPVR shifts to left when contractility increasesESPVR shifts to left when contractility increasesdecreased ejection at any given preload and afterload

ESPVR shifts to right when contractility decreasesincreased ejection at any given preload and afterload

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EDPVRindex of compliance

All EDPV points lie along a line

EDPVR shifts to left and up when ventricular compliance decreasesdiastolic dysfunction

EDPVR shifts to right and down when ventricular compliance increasesdilated cardiomyopathy

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c

d

LVESPVR

100

150

LV P

ress

ure

LV PRESSURE VOLUME CURVE

a-MV opensb-MV closesc-AV opensd-AV closes

a-b = preloadb-c = afterload

LV volume

ab

50 130

50

isov

olem

ic re

laxa

tion

Isov

olem

ic con

trac

tion

LVESDVR

LV P

ress

ure

b-c = afterloadc-d = stroke volume

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Isom

etric

relaxa

tion

Isom

etric

con

trac

tion

Mus

cle tens

ion

End systolic length

CARDIAC MUSLCE LENGTH TENSION CURVE

Muscle length

Isom

etric

relaxa

tion

Isom

etric

con

trac

tion

Mus

cle tens

ion

End diastolic length

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Decreased ventricular contractilityDecreased ventricular contractilitysystolic dysfunction

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c

d

LVESPVR

100

150

Isov

olem

ic con

trac

tion

LV P

ress

ure

Decreased Contractility = ventricular systolic dysfunctionConsidering normal preload, afterload and ventricular compliance

c-d’= stroke volume130-80= 50

d’

c-d= stroke volume130-50= 80

LV volume

ab

50 130

50

isov

olem

ic re

laxa

tion

Isov

olem

ic con

trac

tion

LVESDVR

LV P

ress

ure 130-80= 50

80

a’

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Decreased Contractility = ventricular systolic dysfunction

EF or FS dependent onPreload

Contractility afterload

Increased LVESV: decreased SV and EF

Increased LV end systolic volumewith

Normal or decreased afterload

afterload

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c

LVESPVR

100

150

LV P

ress

ure

Decreased Contractility = ventricular systolic dysfunctionCompensatory response of Nature


d’

Increased SVRIncreased MSFPIncreased VR

Increased LVEDVIncreased HR

c’

LV volume

a’b

50 130

50

LVESDVR

LV P

ress

ure

80

c’-d’= stroke volume150-80= 70

150

b’Increased O2 costPulmonary oedema

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Myocardial ischemia

Decreased Contractility = ventricular systolic dysfunctionCauses:

Acute

Myocardial Intracelluar AcidosisDecreased affinity of Calcium to contractile proteins

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Acute

Respiratory acidosiscauses intracelluar acidosis

Significantly decreases contractility at PaCO2 level of 60Chronic respiratory acidosis leads to metabolic compensation

leading to nearly normal intracellular pH

Metabolic acidosisLess effect as minimal change in intracellular pHOnly 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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Acute

Ionized hypocalcemiaMassive PRBC transfusion: citrate bind to Ca

Lactic acid also binds to CaBicarbonate infusion also decreased Ca

Hypokalemia or hyperkalemiaHypomagnesimiahypophosphatemia

Bicarbonate infusionIncreases PaCO2: decreases intracellular pH

Increased lactic acid production: by increasing rate limiting step of glycolysisDecreases ionized Calcium

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Acute

Proinflammatory cytokinesTNF ᾳ, IL 1, 2, 6

Increased NO production

Reactive oxygen intermediates Released by leucocytes

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Chronic

IdiopathicCoronary artery disease

Inflammatory: viral, toxoplasmosis, chagas diseaseAlcoholicAlcoholic

Infective: HIVPostpartum

UremicDiabetic

Nutritional deficiency: selenium deficiencyMetabolic disorders: fabry disease, Gaucher disease

Toxic: Adriamycin, cobalt

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Decreased Contractility = ventricular systolic dysfunctionManagement

Correcting acute reversible causes

IshemiaAcidosisAcidosis

Dyselectrolytemiahypothermia

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Decreased Contractility = ventricular systolic dysfunctionManagement

Increasing PRELOAD

DecreasingAFTERLOAD

IncreasingCONTRACTILITYPRELOAD AFTERLOADCONTRACTILITY

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Increasing preloadincreasing MSFP: increasing Stress volume

Increased venous tone by sympathetic nervous systemFluid retention by kidneys

Volume optimization

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Cardiac

outpu

t

6

8

10

12

Guytonian Cardiac function Curve

Increasing preloadincreasing MSFP

Pra

Cardiac

outpu

t

-5 0 5 10 15 20

2

4

6

25

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c

LVESPVR

100

150

LV P

ress

ure



d’


c’

LV volume

b

50 130

50

LVESDVR

LV P

ress

ure 160-80= 80

80

a’

b’

160

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Fluidcrystalloid vs colloid

Safety margin: interstitial oedema

Can be increased by

Safety margin: interstitial oedema

vasopressures

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Increasing preloadincreasing 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

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Heart in sepsis, Textbook of Critical Care Medicine, Shoemaker��

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c

LVESPVR

100

150

LV P

ress

ure

Increasing preloadincreasing ventricular compliance


d’


c’

LV volume

b

50 130

50

LVESDVR

LV P

ress

ure 160-80= 80

80

a’ b’

160

LVESDVR’

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Increasing preloadincreasing 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

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Pericardial P- V curve of dead canine heartPpc vs intracardiac volume

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

Intracardiac

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Pericardial P- V curve of isolated dog heartRole of pericardium

Intact pericardium----Intrapericardial volume

…Intracardiac volumePericardium removed( intracardiac volume)

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

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Increasing preloadincrease Pra = increase Ppc = Pulmonary odema

Ponc = 21 21 21 21 21

Ppc = 15 13 11 9 7

Ppc-Ponc = -6 -8 -10 -12 -14

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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 permeabilityIs 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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Increasing preload

In critically ill patients without previous cardiac dysfunction major factor limiting cardiac output is limited venous return

Limited venous returnIncreased venous capacitance: increase unstressed volume

Positive pressure ventilationVentricular diastolic dysfunction

Venous return can be increased withIonotropes 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 evaluatedTo avoid ineffective flogging of empty heart

To avoid flooding of lungs and interstitial tissues

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c

d’’

LVESPVR

100

150

LV P

ress

ure

Decreased Contractility = ventricular systolic dysfunctionIncreasing contractility


d’


LV volume

a’’b

50 130

50

LVESDVR

LV P

ress

ure

80

130-50= 80

a’

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c

LVESPVR

100

150

LV P

ress

ure

Decreased Contractility = ventricular systolic dysfunctionDecreasing afterload


d’

c-d’’= stroke volume130-55= 75

d’’

c’

LV volume

a’b

50 130

50

LVESDVR

LV P

ress

ure

80

130-55= 75

55

a’’

c’

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Decreased ventricular complianceDecreased ventricular compliancediastolic dysfunction

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c

d

LVESPVR

100

150

LV P

ress

ure

Decreased ventricular compliance: diastolic dysfunction

c’ c’-d= stroke volume100-50= 50


LV volume

ab

50 130

50

LVESDVR

LV P

ress

ure

b’

100-50= 50

100

LVESDVR’

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End diastolic volume decreased: decreased SV and EF


EF or FS dependent onPreload

Contractility afterload

decreased LV end diastolic volume

with

Normal or increased Pra/ LVEDP

afterload

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In the absence of EchocardiographyShould be suspected

when decreased LV pump function is not responding tofluid expansion/ vasopressors, ionotropic agents and reduction of afterload


Cardiac output is unusually sensitive to changes in heart rateLate 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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Myocardial ischemiadelayed systolic relaxation leading to stiffness

Diastolic stiffness precedes depressed contractility

Decreased ventricular compliance: diastolic dysfunctionCauses:

Acute

Increased intrathoracic pressureIncreased intrathoracic pressureIncreased intrapericardial pressure

positive pressure ventilation, pneumothorax, massive pleural effusionIncreased intraperitoneal pressure

Catecholemines and calcium infusionhypothermia

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Concentric ventricular hypertrophyHOCM

Decreased ventricular compliance: diastolic dysfunctionCauses:

Chronic

Restrictive CMPConstrictive pericarditis

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Identify Optimal filling pressuresthat maximizes LVEDV without causing substantial pulmonary odema

Treatment of causesIschemia, pneumothorax

Increased pleural, pericardial, abdominal pressuresOptimized intrathoracic pressure in PPV patients: low tidal ventilation strategy

Decreased ventricular compliance: diastolic dysfunctionManagement:

Optimizes volume statuscorrect hypovolemia aggressively and promptly not overlooking safety margin

Optimize Ionotropes and vasopressor dosessmallest dose that achieves desired systolic and vascular effect

Tachycardia, arrhythmias should be treated earlyHypothermia should be avoided

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The The Right Ventricle

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right ventricle is thin walled pump, with large radius of curvatureBuilt 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 volumeallowing it to increase preload

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•Pulmonary embolism•Hypoxic pulmonary vasoconstriction•Acidemic pulmonary vasoconstriction

•ARDS•Sepsis

•Positive pressure ventilation

RV incrased afterload

acute

•Chronic hypoventilation•Recurrent pulmonary embolism

•PPH•Chronically elevated LA pressure: MS, LVF

•Positive pressure ventilation

Chronic

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•Management of ventricular interdependence

•Management of acute cause

RV incrased afterloadManagement

•Management of ventricular interdependenceDecrease parallel coupling of LV and RV

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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

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“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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THANK YOUTHANK YOU

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Date post:	19-Jun-2015
Category:	Education
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Ventricular dysfunction in_critically_ill

Education