ventricular dysfunction in_critically_ill
TRANSCRIPT
![Page 1: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/1.jpg)
Ventricular dysfunction inCritically Ill
������������� ������������������������������������� ����������� ���������������
![Page 2: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/2.jpg)
“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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 3: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/3.jpg)
Ventricular function
PRELOAD AFTERLOADCONTRACTILITY
DIASTOLIC COMPLIANCE
PRELOAD AFTERLOADCONTRACTILITY
VALVE FUNCTION
HEART RATE
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 4: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/4.jpg)
VENTRICULARPRESSURE- VOLUMEPRESSURE- VOLUME
RELATIONSHIP
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 5: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/5.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 6: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/6.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 7: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/7.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 8: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/8.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 9: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/9.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 10: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/10.jpg)
Decreased ventricular contractilityDecreased ventricular contractilitysystolic dysfunction
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 11: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/11.jpg)
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’
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 12: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/12.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 13: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/13.jpg)
c
LVESPVR
100
150
LV P
ress
ure
Decreased Contractility = ventricular systolic dysfunctionCompensatory response of Nature
c-d’= stroke volume130-80= 50
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 14: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/14.jpg)
Myocardial ischemia
Decreased Contractility = ventricular systolic dysfunctionCauses:
Acute
Myocardial Intracelluar AcidosisDecreased affinity of Calcium to contractile proteins
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 15: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/15.jpg)
Decreased Contractility = ventricular systolic dysfunctionCauses:
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 16: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/16.jpg)
Decreased Contractility = ventricular systolic dysfunctionCauses:
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 17: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/17.jpg)
Decreased Contractility = ventricular systolic dysfunctionCauses:
Acute
Proinflammatory cytokinesTNF ᾳ, IL 1, 2, 6
Increased NO production
Reactive oxygen intermediates Released by leucocytes
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 18: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/18.jpg)
Decreased Contractility = ventricular systolic dysfunctionCauses:
Chronic
IdiopathicCoronary artery disease
Inflammatory: viral, toxoplasmosis, chagas diseaseAlcoholicAlcoholic
Infective: HIVPostpartum
UremicDiabetic
Nutritional deficiency: selenium deficiencyMetabolic disorders: fabry disease, Gaucher disease
Toxic: Adriamycin, cobalt
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 19: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/19.jpg)
Decreased Contractility = ventricular systolic dysfunctionManagement
Correcting acute reversible causes
IshemiaAcidosisAcidosis
Dyselectrolytemiahypothermia
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 20: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/20.jpg)
Decreased Contractility = ventricular systolic dysfunctionManagement
Increasing PRELOAD
DecreasingAFTERLOAD
IncreasingCONTRACTILITYPRELOAD AFTERLOADCONTRACTILITY
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 21: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/21.jpg)
Increasing preloadincreasing MSFP: increasing Stress volume
Increased venous tone by sympathetic nervous systemFluid retention by kidneys
Volume optimization
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 22: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/22.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 23: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/23.jpg)
c
LVESPVR
100
150
LV P
ress
ure
Increasing preloadincreasing MSFP
c-d’= stroke volume160-80= 80
d’
c-d= stroke volume130-80= 50
c’
LV volume
b
50 130
50
LVESDVR
LV P
ress
ure 160-80= 80
80
a’
b’
160
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 24: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/24.jpg)
Increasing preloadincreasing MSFP
Fluidcrystalloid vs colloid
Safety margin: interstitial oedema
Can be increased by
Safety margin: interstitial oedema
vasopressures
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 25: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/25.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 26: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/26.jpg)
Heart in sepsis, Textbook of Critical Care Medicine, Shoemaker������������� ��������������� ����������������������� �
�������������� �������� ������
![Page 27: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/27.jpg)
c
LVESPVR
100
150
LV P
ress
ure
Increasing preloadincreasing ventricular compliance
c-d’= stroke volume160-80= 80
d’
c-d= stroke volume130-80= 50
c’
LV volume
b
50 130
50
LVESDVR
LV P
ress
ure 160-80= 80
80
a’ b’
160
LVESDVR’
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 28: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/28.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 29: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/29.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 30: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/30.jpg)
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������������� ��������������� ����������������������� �
�������������� �������� ������
![Page 31: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/31.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 32: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/32.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 33: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/33.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 34: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/34.jpg)
c
d’’
LVESPVR
100
150
LV P
ress
ure
Decreased Contractility = ventricular systolic dysfunctionIncreasing contractility
c-d’= stroke volume130-80= 50
d’
c-d= stroke volume130-50= 80
LV volume
a’’b
50 130
50
LVESDVR
LV P
ress
ure
80
130-50= 80
a’
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 35: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/35.jpg)
c
LVESPVR
100
150
LV P
ress
ure
Decreased Contractility = ventricular systolic dysfunctionDecreasing afterload
c-d’= stroke volume130-80= 50
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’
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 36: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/36.jpg)
Decreased ventricular complianceDecreased ventricular compliancediastolic dysfunction
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 37: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/37.jpg)
c
d
LVESPVR
100
150
LV P
ress
ure
Decreased ventricular compliance: diastolic dysfunction
c’ c’-d= stroke volume100-50= 50
c-d= stroke volume130-50= 80
LV volume
ab
50 130
50
LVESDVR
LV P
ress
ure
b’
100-50= 50
100
LVESDVR’
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 38: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/38.jpg)
End diastolic volume decreased: decreased SV and EF
Decreased ventricular compliance: diastolic dysfunction
EF or FS dependent onPreload
Contractility afterload
decreased LV end diastolic volume
with
Normal or increased Pra/ LVEDP
afterload
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 39: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/39.jpg)
In the absence of EchocardiographyShould be suspected
when decreased LV pump function is not responding tofluid expansion/ vasopressors, ionotropic agents and reduction of afterload
Decreased ventricular compliance: diastolic dysfunction
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)
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 40: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/40.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 41: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/41.jpg)
Concentric ventricular hypertrophyHOCM
Decreased ventricular compliance: diastolic dysfunctionCauses:
Chronic
Restrictive CMPConstrictive pericarditis
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 42: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/42.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 43: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/43.jpg)
The The Right Ventricle
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 44: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/44.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 45: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/45.jpg)
•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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 46: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/46.jpg)
•Management of ventricular interdependence
•Management of acute cause
RV incrased afterloadManagement
•Management of ventricular interdependenceDecrease parallel coupling of LV and RV
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 47: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/47.jpg)
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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 48: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/48.jpg)
“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
������������� ��������������� ����������������������� ��������������� �������� ������
![Page 49: Ventricular dysfunction in_critically_ill](https://reader033.vdocument.in/reader033/viewer/2022042602/55841c4bd8b42a34708b5193/html5/thumbnails/49.jpg)
THANK YOUTHANK YOU
������������� ��������������� ����������������������� ��������������� �������� ������