DO2 = Cardiac output . CaO2 . K DO2 = Cardiac output . Hb . SaO2 . K
CO CO CO
Hb SaO2 Hb SaO2 Hb SaO2
DO2 DO2 DO2 ? low HYPOXEMIA A low PaO2 (regardless the FiO2 )
HYPOXIA Lack of oxygen (in the cell)
DO2 = Cardiac output x Arterial O2 content
hemoglobin SaO2
PaO2 CIRCULATORY FAILURE
Inability for the cells to get enough OXYGEN in relation to their oxygen needs
OXYGEN DELIVERY assessed by the degree of tissue perfusion 2019
INTERPRETATION OF CARDIAC OUTPUT
Convulsions Sepsis Anemia Jogging Agitation Inflammation Hypoxemia Walking Anxiety Standing « normal » Calm value Resting Sedation Sleeping Anesthesia Hypothermia Polyglobulism Do we need to monitor cardiac output during major surgery ?
Vincent JL & Fagnoul D
Anesthesiology 2012 (editorial) Regional SvO2
K Reinhart CARDIAC OUTPUT
HIGH LOW
SvO2 SvO2
NORMAL / HIGH LOW NORMAL / HIGH LOW INFLAMMATION LOW VO2 LOW OUTPUT ( incl. sepsis ) SaO2 / Hb SYNDROME ( anesthesia, PERIPHERAL a) hypovolemia hypothermia,...) SHUNTING b) cardiac pump ( vasodilators, low normal problem cirrhosis ) ANEMIA HIGH VO2 c) obstruction HYPERVOLEMIA HYPOXEMIA (cf exercise) Cardiac output Cardiac output Cardiac output Cardiac output adequate or inadequate adequate or inadequate adequate adequate or inadequate
Pinsky MR & Vincent JL, Crit Care Med 33: 1119, 2005 Vincent et al, Crit Care 15: 229, 2011 CARDIAC OUTPUT fluids how to increase pace-maker
PRELOAD HEART RATE
CONTRACTILITY AFTERLOAD
dobutamine vasodilators PRELOAD
LENGTH OF THE MYOCARDIAL FIBER PRIOR TO CONTRACTION
END-DIASTOLIC VOLUME VENTRICULAR FUNCTION CURVE STROKE VOLUME EDEMA CARDIAC OUTPUT Should we measure ventricular volumes?
END-DIASTOLIC VOLUME PRELOAD PRELOAD AFTERLOAD END-DIASTOLIC PRESSURE
CONTRACTILITY CVP / PAOP VENTRICULAR FUNCTION CURVE
CONTRACTILITY and/or how to better separate STROKE AFTERLOAD the two ? VOLUME x PRESSURE generated by the ventricle INOTROPIC or VASODILATING THERAPY ?
PRELOAD
AFTERLOAD END-DIASTOLIC VOLUME PRELOAD CONTRACTILITY WORK = VOLUME x PRESSURE
VENTRICULAR WORK = k . STROKE VOLUME . D PRESSURE
PAP PAPO
CVP MAP RV LV
LVSWI = k' . SV . (MAP - PAPO)
RVSWI = k' . SV . (PAP - CVP) WORK = VOLUME x PRESSURE
MINUTE WORK = STROKE WORK x HEART RATE
PRELOAD
AFTERLOAD
CONTRACTILITY VENTRICULAR FUNCTION CURVE
STROKE VOLUME descending slope ?
✓ Changes in afterload (vasoconstriction)
PRELOAD END-DIASTOLIC✓ Myocardial VOLUMEischemia AFTERLOAD ✓ RV failure (ventricular interactions) CONTRACTILITY VENTRICULAR FUNCTION CURVE
CONTRACTILITY STROKE and/or VOLUME AFTERLOAD
Stroke volume Ejection fraction = End-diastolic volume
END-DIASTOLIC VOLUME PRELOAD
AFTERLOAD PRELOAD
CONTRACTILITY effects of fluids on ejection fraction
STROKE fluids VOLUME
Fluid infusion can decrease EF
END-DIASTOLIC VOLUME PRELOAD
AFTERLOAD
CONTRACTILITY A DECREASED EJECTION FRACTION does not necessarily imply A DECREASED STROKE VOLUME
SV SV EDV EDV ESV ESV
SV EF = EDV VENTRICULAR DYSFUNCTION
vs.
VENTRICULAR FAILURE VENTRICULAR FUNCTION CURVE
STROKE VOLUME EF DYSFUNCTION
FAILURE
PRELOAD END-DIASTOLIC VOLUME
AFTERLOAD
CONTRACTILITY VENTRICULAR DYSFUNCTION (no reduction in cardiac output) vs.
VENTRICULAR FAILURE (reduction in cardiac output) REGIONAL HYPOXIA HYPERCAPNIA VASCULAR VASCULAR VASOCONSTRICTING OBSTRUCTION COMPRESSION MEDIATORS (thrombosis) (edema) (thromboxane, endothelins...) ENDOTHELIAL POLYCYTHEMIA SWELLING HYPERVISCOSITY PULMONARY HYPERTENSION Increased RV afterload CVP
RV LV
Dilatation Decreased RVEF RAP LAP
NORMAL
3-6 mmHg
RV DYSFUNCTION or FAILURE VENTRICULAR FUNCTION CURVE
STROKE Inhaled VOLUME vasodilators EF DYSFUNCTION Systemic vasodilators FAILURE
END-DIASTOLIC VOLUME RV dysfunction vs failure
The effects of inhaled NO on RV function in ARDS Rossaint et al, Intensive Care Med 21: 197-203, 1995 Fierobe et al, Am J Respir Crit Care Med 151: 1414-9, 1995 Lowson et al, Anesth Analg 82: 574-81, 1996 Rossetti et al, Am J Respir Crit Care Med 154: 1375-81, 1996 Walmrath et al, Am J Respir Crit Care Med 153: 991-6, 1996 Bhorade et al, Am J Respir Crit Care Med 159: 571-9, 1999
Is ARDS usually associated with right ventricular dysfunction or failure? Vincent JL, Intensive Care Med 21: 195-6, 1995 PULMONARY HYPERTENSION
RAP > PAPO PAP > 25 mmHg
MAP < 70 mmHg 70-100 mmHg > 100 mmHg
Norepinephrine Dobutamine Hydralazine (Isoproterenol) PGE1/PGI2
Inhaled NO PULMONARY HYPERTENSION Increased right ventricular filling
CARDIAC OUTPUT
ADEQUATE INADEQUATE (tissue perfusion - SvO2)
RV DYSFUNCTION RV FAILURE
PULM. ART. P. + INHALED NO ? PGE1 ? NORMAL INCREASED
NOTHING ARTERIAL PRESSURE DIURETICS ?
NORMAL LOW
DOBUTAMINE VASODILATORS VASOPRESSORS D PRESSURE RESISTANCE = k BLOOD FLOW WORK = k . VOLUME . D PRESSURE
MAP - CVP PAP PAPO SVR = k. CO PAP - PAPO CVP PVR = k. MAP CO RV LV
LVSWI = k' . SV . (MAP - PAPO)
RVSWI = k' . SV . (PAP - CVP) INTERPRETATION OF CARDIAC OUTPUT
High CO Low CO
High filling High filling
yes no yes no cardiac pump hypovolemia Hypervolemia inflammation (sepsis ?) problem low VO2 cirrhosis anemia hypoxemia tamponade pulm. embolism PRELOAD HOW TO INFLUENCE CARDIAC OUTPUT AFTERLOAD
CONTRACTILITY
Filling pressures What was Cardiac output Ventricular volumes the intervention ?
Increased Fluids Increased Stable or Dobutamine decreased or vasodilators
Decreased Diuretics / UF Decreased Stable or Beta-blocking agent increased (or pure vasoconstrictors) How to interpret a cardiac output ?
Filling
SvO2
brain muscle skin can be liver evaluated kidneys clinically GI tract VENTRICULAR FUNCTION CURVE
ADRENERGIC HYPERVOLEMIA CARDIAC RESPONSE OUTPUT
CARDIAC HYPOVOLEMIA FAILURE
PRELOAD CARDIAC FILLING AFTERLOAD
CONTRACTILITY CARDIAC OUTPUT
FLUIDS PACEMAKER
PRELOAD HEART RATE
AFTERLOAD CONTRACTILITY DOBUTAMINE VASODILATORS The determinants of cardiac output
ICU nephrology: the implications of cardiovascular alterations in the acutely ill Vincent JL & De Backer D, Kidney Intern 81: 1060-6, 2012 HOW TO GO FASTER ON A BICYCLE
PRELOAD changing gears
HEART RATE
CONTRACTILITY AFTERLOAD How to increase cardiac output Crit Care 12: 174, 2008; Kidney Int 81: 1060-1066, 2012 CHANGING HEART RATE HOW TO GO FASTER ON A BICYCLE
PRELOAD
wind HEART RATE
CONTRACTILITY AFTERLOAD How to increase cardiac output Crit Care 12: 174, 2008; Kidney Int 81: 1060-1066, 2012 fluids STROKE VOLUME
PRELOAD (end-diastolic volume) FLUID CHALLENGE vs DIURETICS
CARDIAC STOP DIURETICS OUTPUT
? DIURETICS
OK DIURETICS
EDEMA
PAPO HOW TO GO FASTER ON A BICYCLE
PRELOAD
HEART RATE pushing harder
CONTRACTILITY AFTERLOAD How to increase cardiac output Crit Care 12: 174, 2008; Kidney Int 81: 1060-1066, 2012 INFLUENCING THE BETA-ADRENERGIC SYSTEM
beta-stimulation beta-blockade (dobutamine) lower CO higher CO lower LVSWI higher LVSWI lower SvO2 higher SvO2 slower heart rate faster heart rate vasoconstriction vasodilation
CO CO
DOSES DOSES HOW TO GO FASTER ON A BICYCLE
PRELOAD
INCREASE acutely HEART RATE to increase DO2
CONTRACTILITY AFTERLOAD DECREASE chronically to protect the heart HOW TO GO FASTER ON A BICYCLE
PRELOAD
HEART RATE
Smooth road CONTRACTILITY AFTERLOAD How to increase cardiac output Crit Care 12: 174, 2008; Kidney Int 81: 1060-1066, 2012 VASODILATORS veins arteries
nitrates hydralazine sodium nitroprusside alpha-blocking agents ACE inhibitors vasodilator STROKE therapy VOLUME
Normal
Heart failure
AFTERLOAD D pressure RESISTANCE = flow MPAP - PAOP PVR = CO
MAP - RAP SVR = CO RV LV HEMODYNAMIC EFFECTS OF VASOACTIVE AGENTS Resistance (vascular tone)
vasopressors ARTERIAL PRESSURE vasodilators inotropes
CARDIAC OUTPUT AFTERLOAD CHANGES
vasopressors vasodilators
lower CO higher CO higher art. pressure lower art. pressure higher CPP increased ICP
CO CO
AFTERLOAD AFTERLOAD HOW TO GO FASTER ON A BICYCLE
PRELOAD
IV fluids Pacemaker
HEART RATE
Vasodilators CONTRACTILITY AFTERLOAD Dobutamine How to increase cardiac output Crit Care 12: 174, 2008; Kidney Int 81: 1060-1066, 2012 INOTROPIC EFFECTS OF ANTIHYPERTENSIVE AGENTS
HYDRALAZINE + NITROPRUSSIDE CALCIUM ANTAGONISTS BETA-BLOCKING AGENTS - Message
A low cardiac output is always associated with a low DO2
BUT A high cardiac output is NOT always associated with a high DO2 When you measure a high cardiac output do not say: "cardiac output is 'fine'…" SOME APPLICATIONS
Heart failure Circulatory shock Sepsis Transfusions Arterial hypertension STROKE STROKE VOLUME VOLUME
NORMAL
HEART FAILURE
AFTERLOAD PRELOAD PRELOAD
AFTERLOAD
CONTRACTILITY HEART FAILURE
PRELOAD
HEART RATE
CONTRACTILITY AFTERLOAD Adrenergic Renin-angiotensin Vasopressin VASODILATORS
PRELOAD HEART RATE adrenergic response
CONTRACTILITY AFTERLOAD CALCIUM ANTAGONISTS
PRELOAD HEART RATE adrenergic response
CONTRACTILITY AFTERLOAD CALCIUM ANTAGONISTS HYDRALAZINE
PRELOAD HEART RATE adrenergic response
CONTRACTILITY AFTERLOAD VASODILATORS « INODILATORS »
PRELOAD HEART RATE
CONTRACTILITY AFTERLOAD SOME APPLICATIONS
Heart failure Circulatory shock Sepsis Transfusions Arterial hypertension Vasodilators for heart failure Arterial pressure = cardiac output x vascular tone
Vasopressors for hypotension Arterial pressure = cardiac output x vascular tone
b a Norepinephrine in shock SHOCK MANAGEMENT
CARDIAC OUTPUT
PRELOAD HEART RATE Fluids
AFTERLOAD Vasopressors
CONTRACTILITY Norepinephrine Dobutamine
VASCULAR TONE PHENYLEPHRINE or VASOPRESSIN
Arterial pressure = Cardiac output x Resistance
HEART RATE PRELOAD (baroreflex)
CONTRACTILITY AFTERLOAD SOME APPLICATIONS
Heart failure Circulatory shock Sepsis Transfusions Arterial hypertension HEMODYNAMIC ALTERATIONS IN SEPSIS
HIGH LOW
Arterial pressure = cardiac output x resistance CARDIOVASCULAR ALTERATIONS IN SEPSIS
High SvO2 High CO
Low SVR
Endothelial Circulating dysfunction vasoactive Vasodilation substances
Microvascular Decreased cell obstruction deformability SEPSIS “Mediators” (vasoactive substances)
Distributive defect (microcirculatory alterations) Vasodilatation High plasma volume High cardiac output High SvO2 ALTERED MYOCARDIAL FUNCTION IN SEPTIC SHOCK
Decreased coronary perfusion ?
Microvascular Direct effects alterations TNF prostaglandins thromboxane thromboxane PAF PAF adenosine adenosine heat shock proteins angiotensin sphingosine kinins O2 free radicals O2 free radicals NO NO adhesion molecules TNF IL-1...
PAF sphingosine iNOS direct O2 free effects radicals caspases calcium release NO - ONOO cGMP apoptosis decreased calcium sensitivity
Decreased contractility SEPTIC SHOCK IS CHARACTERIZED BY A NORMAL/HIGH CARDIAC OUTPUT
QUESTION
HOW IS IT COMPATIBLE WITH MYOCARDIAL DEPRESSION ? SEPTIC SHOCK a normal/high cardiac output does not exclude myocardial depression
PRELOAD HEART RATE
CONTRACTILITY AFTERLOAD a normal/high cardiac output SEPSIS does not exclude some myocardial depression
PRELOAD
HEART RATE
CONTRACTILITY AFTERLOAD SEPTIC SHOCK IS CHARACTERIZED BY A NORMAL/HIGH CARDIAC OUTPUT
QUESTION HOW CAN WE IDENTIFY MYOCARDIAL DEPRESSION IN SEPTIC PATIENTS ?
ANSWER
1- LVSWI / RVSWI 2- Ejection fractions MYOCARDIAL DEPRESSION CHARACTERIZES THE FATAL COURSE OF SEPTIC SHOCK Surgery 111: 660-7, 1992 Survivors Non-survivors RVSWI LVSWI gm/M² gm/M² 10 40
8 30
6 20 4
10 2
0 0 INITIAL FINAL INITIAL FINAL MYOCARDIAL DEPRESSION IN SEPSIS DECREASED EJECTION FRACTION
SV SV EDV EDV ESV ESV
SV EF = EDV
Parker et al, Ann Intern Med 100: 483-90, 1984 MYOCARDIAL DEPRESSION IN SEPSIS
THE SEVERITY OF MYOCARDIAL DEPRESSION AS REFLECTED BY THE LEFT VENTRICULAR EJECTION FRACTION
NOT RELATED TO OUTCOME ?
Parker et al, Ann Intern Med 100: 483-90, 1984 SEPTIC SHOCK
MEDIATORS
MYOCARDIAL CIRCULATORY DEPRESSION ALTERATIONS low ejection fraction low SVR low ventricular stroke work altered oxygen extraction MYOCARDIAL DEPRESSION IN SEPSIS
IF MEDIATORS ARE INVOLVED IN THE SEPSIS-RELATED MYOCARDIAL DEPRESSION then THE MORE SEVERE THE SEPSIS THE MORE SEVERE THE MYOCARDIAL DEPRESSION
then
THE MYOCARDIAL DEPRESSION MUST BE MORE SEVERE IN THE NON-SURVIVORS THAN IN THE SURVIVORS RIGHT vs LEFT VENTRICULAR FUNCTION IN SEPSIS
increased afterload (high PVR, high PAP)
RV LV
Decreased contractility decreased afterload (low SVR, low AP) MYOCARDIAL DEPRESSION CHARACTERIZES THE FATAL COURSE OF SEPTIC SHOCK Surgery 111: 660-7, 1992 68 patients with septic shock 38 survivors 30 non-survivors RVEF determined by the thermodilution technique MYOCARDIAL DEPRESSION CHARACTERIZES THE FATAL COURSE OF SEPTIC SHOCK Surgery 111: 660-7, 1992 MAP, mmHg MPAP, mmHg CI, L/min.M² 75 30 4 70 65 25 3 60 20 2 55 50 15 1 45 40 10 0 PAOP, mmHg RAP, mmHg 16 16
12 12
8 8 Survivors Non-survivors 4 4
0 0 MYOCARDIAL DEPRESSION CHARACTERIZES THE FATAL COURSE OF SEPTIC SHOCK Surgery 111: 660-7, 1992 Stroke index, mL/M² RVEF, % MPAP, mmHg 35 50 30 30 40 25 p<0.01 25 20 30 15 20 20 10 5 10 15 0 0 10
RVEDVI, mL/M² RVESVI, mL/M² 70 100 60 90 p<0.05 p<0.01 80 50 70 40 Survivors 60 30 Non-survivors 50 20 SEPTIC SHOCK a normal/high cardiac output does not exclude myocardial depression
PRELOAD HEART RATE
CONTRACTILITY AFTERLOAD
SURVIVORS
NON-SURVIVORS THE MORE SEVERE THE SEPSIS
THE GREATER THE RELEASE OF MEDIATORS
THE MORE SEVERE THE MYOCARDIAL DEPRESSION
THE MORE SEVERE THE CIRCULATORY ALTERATIONS SURVIVING SEPSIS CAMPAIGN
2016
VASOACTIVE AGENTS
We suggest using dobutamine in patients who show evidence of persistent hypoperfusion despite adequate fluid loading and the use of vasopressor agents.
Grade 2C
Crit Care Med 2017 Intensive Care Med 2017 SOME APPLICATIONS
Heart failure Circulatory shock Sepsis Transfusions Arterial hypertension Hemorrhage
Normovolemic anemia HEMORRHAGE
HYPOVOLEMIA ANEMIA
FLUIDS TRANSFUSION HOW HEMOGLOBIN LEVELS FALL Bleeding
Blood
Lower Hb
IV fluids transcapillary refill ANEMIA DUE TO HEMODILUTION ? Hemodilution "adequate" Blood volume increased (by 15 % ?) blood volume
IV fluids
"adequate" "iatrogenic" ? Decreased RBC mass blood volume IV fluids More common !
anemia "revealed" after fluid administration RESPONSE TO HEMODILUTION
INCREASE IN CARDIAC OUTPUT REDUCED BLOOD VISCOSITY ✓ Increased venous return ✓ Decreased ventricular afterload SYMPATHETIC RESPONSE ✓ Increased myocardial contractility ✓ Tachycardia BLOOD FLOW REDISTRIBUTION towards heart & brain
INCREASED OXYGEN EXTRACTION Capillary recruitment Improved blood flow distribution in the capillaries OXYGEN DELIVERY
DO2 = Cardiac output x Arterial O2 content
hemoglobin SaO2
Transfusion TRANSFUSIONS Decreased PRELOAD adrenergic response
HEART RATE
CONTRACTILITY AFTERLOAD
Like a beta-blocking agent that does not decrease DO2 Death /MI
Restrictive Liberal THE HEART IN ANEMIA
Increasedincreased contractility contractility Decreased lower ventricular ventricular afterload afterload Tachycardia faster heart rate Increased oxygen demand relative increase in decreased Relative coronary increase bloodin flow arterial oxygen content coronary blood flow content Decreased oxygen content SOME APPLICATIONS
Heart failure Circulatory shock Sepsis Transfusions Arterial hypertension MANAGEMENT OF HYPERTENSION
Arterial pressure = cardiac output x resistance ARTERIAL HYPERTENSION
CARDIAC OUTPUT ?
PRELOAD HEART RATE
AFTERLOAD
CONTRACTILITY VASCULAR TONE MANAGEMENT OF HYPERTENSION
HIGH HIGH
Arterial pressure = cardiac output x resistance
Hyperadrenergic High cardiac state Filling pressures
Treat the cause Diuretics Beta-blockade Ultrafiltration ? ARTERIAL HYPERTENSION Treat the cause CARDIAC OUTPUT Diuretics Ultrafiltration ? PRELOAD HEART RATE HYPERVOLEMIA
AFTERLOAD
CONTRACTILITY VASCULAR TONE ARTERIAL HYPERTENSION Treat the cause CARDIAC OUTPUT
PRELOAD HEART RATE
ADRENERGIC AFTERLOAD STATE
CONTRACTILITY Beta-blockers ? VASCULAR TONE FLUID CHALLENGE vs DIURETICS
CARDIAC STOP DIURETICS OUTPUT
? DIURETICS
OK DIURETICS
EDEMA
PAPO MANAGEMENT OF HYPERTENSION
HIGH HIGH
Arterial pressure = cardiac output x resistance
Vasodilators ARTERIAL HYPERTENSION Treat the cause CARDIAC OUTPUT
PRELOAD HEART RATE
AFTERLOAD
Vasodilators CONTRACTILITY VASCULAR TONE VASOCONSTRICTION VASODILATORS veins arteries
nitrates hydralazine sodium nitroprusside alpha-blocking agents ACE inhibitors VENTRICULAR FUNCTION CURVE STROKE + INOTROPIC or VOLUME VASODILATING
- INOTROPIC or VASOCONSTRICTING
END-DIASTOLIC VOLUME PRELOAD PRELOAD AFTERLOAD
CONTRACTILITY VASODILATORS
PRELOAD HEART RATE adrenergic response
CONTRACTILITY AFTERLOAD MANAGEMENT OF HYPERTENSION
+ Cardiac function
Beta-blockade - Hydralazine ? NTP / Nitrates Calcium antagonists
+ diuretics ? HYPERTENSIVE CRISES
IV therapy INOTROPICDoses EFFECTS
Sodium nitroprusside 20 None- 300 mcg/min Labetalol (Trandate) 20-Negative50 mg or esmolol (Brevibloc) or 2-20 mg/min Nicardipine (Rydene) 2-5Slightly mg/h negative Hydralazine (Nepresol) 10-Slightly25 mg qpositive 4-6 hours Urapidil 25-None50 mg Increased Increased PRESSURE vascular resistance cardiac work + Volume loading Vasoconstriction Adrenergic stimulation Exercice / pain - + FLOW Cardiac pump failure Cirrhosis Hypovolemia Vasodilation Tamponade / pulm emb. Distributive shock
Decreased - Decreased cardiac work vascular resistance Increased Increased PRESSURE vascular resistance cardiac work NOREPINEPHRINE PHENYLEPHRINE +
VASOPRESSIN EPINEPHRINE ANGIOTENSIN - DOBUTAMINE +
FUROSEMIDE FLOW ISOPROTERENOL BETA-BLOCKING AGENTS VASODILATORS
Decreased - Decreased cardiac work vascular resistance