Low cardiac output syndrome (LCOS) is a transient reduction in cardiac output that can occur after cardiac surgery if not recognized and managed promptly. It can lead to multi-organ dysfunction and increased mortality. LCOS is caused by factors that decrease contractility, heart rate, preload, or afterload. It is assessed using physical exam, hemodynamics, labs, and echocardiography. Management involves optimizing preload, rhythm, afterload reduction, and use of inotropes like dobutamine or milrinone. Phosphodiesterase inhibitors and levosimendan are also used to increase contractility while reducing preload and afterload.

1. Low cardiac output syndrome in
cardiac surgery
Dr jeevraj rajawat

2. LCOS
• A transient and often reversible reduction in cardiac
output–low cardiac output state (LCOS) with an
associated decrease in systemic oxygen delivery
often occurs following cardiac surgery
• The LCOS if not recognized in time and managed
appropriately may be “progressive” leading to multi -
organ dysfunction, increased morbidity, prolonged
ICU and hospital stay, and even mortality.

3. CO & its determinants
• CO = HR X SV
• = HR X (EDV – ESV)
• ↓ ↓
• Preload Afterload
• Distentibility Contractility
• Preload is the dominant regulator of CO in
normal cardiovascular system but afterload
dominates flow regulation when myocardium is
failing

4. Determinants of Cardiac Output-
cascade of events
DEC VENT
CONTRACTILITY
DEC VENT
PRELOAD
VENOUS
CONSTRICTION
ARTERIAL
CONSTRICTION
VENT OUTFLOW
IMPEDANCE – AFTERLOAD
INC
DEC CARDIAC
PUTPUT
DEC LVEDP
ISCHEMIA INC O2
DEMAND
INC SYMPTH NS
ACTIVITY
INC HR
# O2 DEMAND
SUPPLY
INC WALL
TENSION

5. Etiology

6. Etiology
ed Contractility
• ed ejection fraction
• poor intraoperative myocardial protection
 incomplete myocardial revascularization
 Anastomotic stenosis
 Coronary A. stenosis
• Hypoxia , hypercarbia acidosis

7. Rythym
 Tachycardia will reduced cardiac filling time
 Bradycardia
 Atrial arrhtymias with loss of artial contraction
 Ventricular arrythmias

8. Factors Influencing LCOS
Preoperative
Intra operative
Postoperative

9. Preoperative factors
• Age
• Hypoxia
• cyanotic HEART appear to be more susceptible to ischemia and re-
perfusion injury than normal hearts.
• Hypertrophy
• Ischemia ---------myocardial dysfunction.
• Left to right shunts
• Large L R shunts -----------------postoperative LCOS when the left
ventricular run-off across the VSD is closed

10. Intra Operative Factors
Hypertrophic myocardium….more risk
Sudden decreased SVR as after induction may lead to a spell in cyanotic patients.
inadequate Myocardial protection during cardiac surgery
CPB mediated
Avoid Factors associated with myocardial injury during CPB
Persistent VF
Ventricular distension
Coronary embolism
Reperfusion
Aortic cross clamp
Long aortic cross clamp leads to more chances of reperfusion injury -------------a direct
predictor of postoperative LCOS and death

11. Factors Influencing LCOS (POSTOP)
 Preload
 After load
 Contractility
 Heart rate & rhythm
 Residual lesions (pulm regurg after transannular patch repair of TOF
 Residual VSD
 Residual outflow obstruction )
 All predispose to post op LCOS d/t vol & pressure overload on the
myocardium
 Pulmonary factors like tension pneumothorax
 Pulmonary hpertension crisis
 Extra cardiac causes like temponade
 Severe sepsis

12. Assessment
Bedside physical examination (breath sounds,
murmurs, warmth of extremities, peripheral pulses)
Hemodynamic measurements: assess filling
pressures & determine CO with PAC, calculate SVR,
measure SvO2
ABG (hypoxia, hypercarbia, acidosis/alkalosis),
hematocrit (anemia), and serum potassium (hypo or
hyperkalemia)

13. Assessment of lcos
• Pulse Rate – tachycardia
volume – low
• Blood pressure - borderline or low
• Skin - pale, cool to touch
• Rapid shallow breathing
• Urine output <1ml/kg/hr
• Reduced peripheral temperature
• Capillary refill
May be useful marker of hypovolemia and myocardial
function
• Core temp vs peripheral temp difference is >3
degrees associated with LCO

14. Non Invasive monitoring
• Chest X-ray
• ECG
• Urine Output
• Chest tube Drainage (Mediastinal Bleeding)
• Echocardiography

15. Invasive monitoring
• Arterial blood pressure
• Central venous pressure
• Left atrial pressure
• Thermodilution catheters
• ABG
• Mix venous blood gases

16. Role of Echocardiography
Intraoperative and postoperative transoesophageal
echocardio graphy (TOE) and postoperative transthoracic
echocardiography enable bedside visualization of the heart.
Echo cardio graphy may immediately identify causes of cardio
vascular failure, including cardiac and valvular dysfunction,
obstruction of the RV (pulmonary embolism) or LV outfl ow
tract (for example, systolic anterior motion of the anterior
mitral valve leafl et), or obstruction to cardiac filling in
tamponade.
It might diff erentiate between acute right, left and global HF
as well as between systolic and diastolic dysfunction.

17. Monitoring Of Low CO State
Central venous, pulmonary artery, RA and LA Pressures
Central venous or right atrial lines -------- RV filling or preload in the presence
of AV concordance.
Low CVP indicate inadequate preload ----- Need for volume
High CVP indicate Fluid overload
Diminished RV systolic or diastolic
function (in the absence of TV disease or shunts)
Persistently elevated PAP in relation to systemic BP---- RV dysfunction
Continuous CO measurement to diagnose LCOS
PA catheter,
FloTrac,
Picco

18. LACTATE IN Low CO State
In LCOS there is impaired global perfusion which cause
anaerobic metabolism and ↑ metabolic acidosis.
Serial ABG analysis reveal ↑ levels of base deficit and ↓ HCO3-
levels
↑ in arterial lactate levels from 2 to 8 mmol/L; remaining near
8mmol/l for 2 hrs or more ↓ survival to 10% in acute LOS.
Normal plasma values for lactate 0.7-2.1 meq/l.
Mild to moderate metabolic acidosis 5 meq/L
Severe metabolic acidosis 10 meq/L

19. Mixed Venous Oxygen saturation
• It is percentage of oxygen bound to hb in
blood returning to the right heart
• Normal is > 70 %
• Useful index of circulatory adequacy it reflects
to some extent near tissue oxygen levels.
• Relation b/w CO & SVO2 is not linear; a ↓ in
SVO2 ----------proportionately larger ↓ in CO
• Sample for SVO2 should be taken from PA
catheter or central vein

20. MANAGEMENT OF HEMODYNAMIC PROBLEMS
BP PCWP CO SVR Plan
↓ ↓ ↓ ↓ Volume
N ↑ N ↑ Diuretic
↓ ↑ ↓ ↑ Inotrope
↑ ↑ ↓ ↑ Vasodilator
V ↑ ↓ ↑ Ino/vaso/IABP
↓ N N ↓ Alpha-agent

21. Management------------
 Optimize preload – + & curvilinear relation b/w EDV & contractility &
appropriate vol loading remains the easiest, most rapid & most effective method
of improving CO & tissue perfusion
a) Ideal LA pressure
Pts with preserved Pts with poor
LV function LV function
↓ ↓
15 mmHg Low 20’s
(Stiff hypertrophied LV with diastolic dysfunction
Small LV Chamber –MS: after LV
resection
Pre existing pulm HTN from MV ds)

22. Management------
b) Response to volume infusion
• Failure of filling pressures to rise with
volume
Capillary leak present in the early postop
period
Vasodilatation associated with re-
warming
• Rise in filling pressures without ↑ CO
INOTROPIC SUPPORT NECESSARY
• Harmful effects of excessive preload
- LV wall tension ↑  myocardial ischemia
(↓ Trans – myocardial gradient for CBF
↑ myocardial o2 demand.)
- Interstitial edema of lungs
V/Q abnormalities
hypoxemia
- Systemic venous HTN ↓ Perfusion pressure to
other organs.
Kidneys – diuresis
GIT – splanchnic congestion
Brain – mental state altered

23. Heart Rate and Rhythm
• Sinus rhythm and optimal heart rate are essential.
• the tachycardia limits diastolic filling of the ventricle
and may reduce coronary blood flow to the left
ventricle. Atrial pacing can be beneficial if the patient
has a slow sinus rate.
• Sequential atrioventricular pacing may be necessary if
the rhythm is other than sinus.
• Synchrony between the atria and ventricles becomes
particularly important in the postbypass setting
because ventricular compliance is poor and ventricular
filling becomes more dependent on the atrial kick

24. Afterload reduction
Vasodilators cause reduction in LV afterload will improve cardiac
output, as long as an adequate diastolic pressure is maintained for
coronary perfusion
Marginal C.O------avoid hypotension
Poor C.O-----------------Cautions use of Vasodilators coz ↑ SVR
from intense vasoconstriction is a compensatory mechanism to
maintain perfusion to vital organs.
( SVR > 1500, vasodilators indicated

25. Ionotropic support in locs
• Among catecholamines, consider low-to-moderate doses of
dobutamine and epinephrine: they both improve stoke volume and
increase heart rate while PCWP is moderately decreased;
catecholamines increase myocardial oxygen consumption
• Milrinone decreases PCWP and SVR while increasing stoke volume;
milrinone causes less tachycardia than dobutamine
• Levosimendan, a calcium sensitizer, increases stoke volume and
heart rate and decreases SVR
• Norepinephrine should be used in case of low blood
pressure due to vasoplegia to maintain an adequate
perfusion pressure. Volaemia should be repeatedly
assessed to ensure that the patient is not hypovolaemic
while under vasopressors

26. Choice of ionotrops
• when stoke volume was increased comparably,
dobutamine increased heart rate more than
epinephrine.
• Epinephrine, dobutamine and dopamine all
increase myo cardial oxygen consumption
(MVO2) postoperatively
• However, only with dobutamine is this matched
by a proportional increase in coronary blood flow
suggesting that the other agents may impair
coronary vasodilatory reserve postoperatively.

27. Phosphodiesterase III inhibitors
• Phosphodiesterase III inhibitors, such as amrinone, milrinone or
enoximone, are all potent vasodilators that cause reductions in
cardiac filling pressures, pulmonary vascular resistance and SVR
• they are commonly used in combination with β1-adrenergic
agonists.
• Compared to dobutamine in postoperative low CO,
phosphodiesterase III inhibitors caused a less pronounced increase
in heart rate and decreased the likelihood of arrhythmias also, the
incidence of postoperative myocardial infarction was signifi cantly
lower with milrinone compared to dobutamine
• This could be explained by phosphodiesterase III inhibitors
decreasing LV wall tension without increasing MVO2, despite
increases in heart rate and contractility, in contrast to
catecholamines

28. Levosimendan
• Calcium sensitising inodilator
• Inc CO by improving both stroke volume &HR and dec preload and
afterload
• Dose 12 µg/kg over 10 min, 0.1 µg/kg/min
• Levosimendan has been recommended for the treatment of acute
HF and was recently used for the successful treatment of low CO
after cardiac surgery
• Th e eff ects of levosimendan have been compared to those of
dobu tamine and milrinone . Levosimendan has been shown to
decrease the time to extubation com pared to milrinone .Compared
to dobutamine, levosimendan decreases theincidence of
postoperative atrial fi brillation andmyocardial infarction, ICU
length of stay , acuterenal dysfunction, ventricular arrhythmias, and
mortality in the treatment of post operative LV dysfunction.
• .

29. refractory hypotension – vasoplegia
MAP< 50,
Low filling pressures – CVP < 5, PCWP<10
Normal or elevated CI >2.5L/min/m2
Low SVR < 800
Vasopressor
Methylene blue 1.5 – 2mg/kg
Vasopressin 0.1- 0.4 U/min

30. Calcium Chloride
• Provides ionized Ca2+ which produces a
strong but transient inotropic effect if
hypocalcaemia is present and more sustained
↑SVR even if normocalcemia is present
• Dose : 0.5 -1g slow iv

31. Tri lodo thyronine (T3)
• ↑ CO & ↓ SVR in patients with depressed ventricular
function.
• Randomized studies have not demonstrated a ↓ in
inotropic requirement or an improvement in overall
outcome with use of T3 upon weaning from CPB.
• It may ↓ incidence of post-op AF through an unknown
mechanism.
• Current role of ------as salvage when CPB cannot be
terminated with maximal inotropic support and IABP.
• Dose : 0.05 – 0.08 ug/kg iv

32. Other drug
• Nesritide
• Recombinant B type natriuretic peptide
• ↓ sympathetic responses & inhibits neurohumoral
response in HF
• ↓ preload (PAP) & afterload (SVR)
• Indirectly inc CO without inc HR or myocardial O2
demand
• lusitropic, dilates native coronaries, arterial conduits,
has no proarrhythmic activity
• Dilates renal afferent & efferent arterioles, inc GFR –
strong diuretic synergistic with loop diruretics

33. PAH CRISIS AND LCOS
• optimal sedation
• -neuromuscular blockade
• -induced respiratory or metabolic
alkalosis
• -hyper-oxygenation
• -Avoiding or ablating stimuli
• (trigger pulmonary hypertensive
crises(e.g. administering fentanyl
bolus prior to airway suction).
• -Nitric oxide

34. Mechanical circulatory support
• In case of heart dysfunction with suspected
coronary hypoperfusion, IABP is highly
recommended
• Ventricular assist device should be considered
early rather than later, before end organ
dysfunction is evident
• Extra-corporeal membrane oxygenation is
solution as a bridge to recovery or decision
making

35. IABP
IABP is the fi rst choice device in intra- and perioperative
cardiac dysfunction.
Its advantages include easy insertion , the modest
increase in CO and coronary perfusion, with low
complication rate.
IABP’s main mechanism of action is a reduction
of afterload and increased diastolic coronary perfusion
via electro cardiogram triggered counterpulsation.
IABP reduces heart work and myo cardial oxygen
consumption, favourably modifying the balance of oxygen
demand/supply

36. Extra-corporeal membrane
oxygenation
• Extra-corporeal membrane oxygenation (ECMO)
is increa singly used for temporary mechanical
circulatory support
• Indications include all types of ventricular failure,
for example, intraoperative or postoperative low
CO syn drome, severe acute myocardial
infarction, and cardiac resusci tation.
• An additional advantage is its versatile use not
only in LV, RV or biventricular support, but also
for respiratory assistance and even renal support
by addition of a haemofilter

37. • Thank you