Low cardiac output syndrome- minati

Low Cardiac Output Syndrome, what we can

Do???

Dr. Minati ChoudhuryProfessor

Department of cardiac AnaesthesiaAIIMS

New Delhi

Why to measure CO???

CO—the primary determinant of global O2 transport No absolute value that reflect circulatory adequacy A low CO is clearly detrimental

Achievement of satisfactory cardiac output is the primary aim cardio vascular management during the post operative scenario and ICU management

Satisfactory cardiac output?----

Cardiac index > 2 l/min/m2

Left sided filling pressures < 20mmHg

HR < 100/min

Warm well perfused extremities

Good urine output

Low cardiac output CI < 2 L/min/m2

Left sided filling pressures >20mmHg

SVR >1500dynes/sec/cm5

Requirement of IABP / inotropic support for more than 30 min in ICU to maintain SBP >90mmHg & CI > 2.2 L/min/m2

JCTVS 1996;112:38-51

CO & its determinants

CO = HR X SV= HR X (EDV – ESV)

↓ ↓

Preload AfterloadDistentibility Contractility

Preload is the dominant regulator of CO in normal cardiovascular system but afterload dominates flow regulation when myocardium is failing

CO & its determinants

CO & its determinantsLUSITROPISM Abnormality of myocardial relaxation(Characteristic of aging

myocardium)

Diastolic dysfunction – ↓ diastolic complaince----- impaired systolic relaxation-------------inappropriate tachycardia

End result is LCOS with a small LV chamber at end diastole yet high filling pressures

ACE inhibitors improve diastolic compliance; lusitropicdrugs (CCB) improve impaired systolic relaxation; bradycardiac drugs (BB &CCB) correct inappropriate tachycardia & diuretics ↓ myocardial edema ------------improve compliance.

Determinants of Cardiac Output- cascade of events that worsens in a cyclic fashion ;begins with derangement of any one of the determinants of CO

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

EtiologyDec left vent preload

• Hypovolemia , bleeding vasodilatations for weaning, narcotics, sedatives

• Cardiac tamponade

• PPV & PEEP

• Rt. vent. dysfunction (RV infarction, Pul. HTN)

• Tension pneumothorax

Etiology

ed Contractility

• ed ejection fraction

• Myocardial stunting , ischemic / infarction poor intraoperative myocardial protection incomplete myocardial revascularization Anastomotic stenosis Coronary A. stenosis

• Hypoxia , hypercarbia acidosis

Etiology

Tachycardia & Bradycardia

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

Etiology

ed after load• Vasoconstriction• Fluid overload

Diastolic dysfunction ( common finding after cardioplegic arrest)

EtiologySyndrome ass. with CV instability and hypotension.

• Sepsis ( Hypotension with ed SVR)

• Anaphylactic reaction (blood products , drugs)

• Adrenal insufficiency (primary or pt with preoperative steroids)

• Protamine reaction

Etiology

• Neurogenic Shock

Spinal anaesthesia

Direct damage to the vasomotor center of medulla

Altered function of the vasomotor center in response to low blood glucose( insulin shock)

Action of trainquilizers,narcotics or sedatives

Spinal cord injury

• Vasoplegic symptoms during liver transplantation

Factors Influencing LCOS

Preoperative

Intra operative

Postoperative

Factors Influencing LCOS-------Preoperative factors

• Age

Extremes of age

• Hypoxia

Experimental -----hearts of animals made cyanotic appear to be more susceptible to ischemia and re-perfusion injury than normal hearts.

• Hypertrophy

• Ischemia ---------myocardial dysfunction.

• Left to right shunts Large LR shunts -----------------postoperative LCOS

when the left ventricular run-off across the VSD is closed.

Factors Influencing LCOS------- Intra Operative Factors

• Anesthetic induction

Major surgery and cardiac surgery Hypertrophic myocardium….more risk

• Hypotension

Sudden decreased SVR as after induction may lead to a spell in cyanotic patients.

• Myocardial preservation …… cardiac surgery

• CPB Avoid Factors associated with myocardial injury during CPB

Persistent VF

Ventricular distension

Coronary embolism

Reperfusion

• Aortic cross clamp

Long aortic cross clamp -------------more chances of reperfusion injury -------------a direct predictor of postoperative LCOS and death.

Factors Influencing LCOS--------------Post Operative Factors

Preload After load Contractility Heart rate & rhythm Residual lesions (pulm regurg after transannular patch repair

of TOFResidual VSDResidual outflow obstruction )

All predispose to post op LCOS d/t vol & pressure overload on the myocardium

Pulmonary factors Extra cardiac causes

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)

Assessment

• Agitation• Pulse Rate – tachycardia

volume – low• Blood pressure - borderline or low• Skin - pale, cool to touch• Rapid shallow breathing• Mucus membranes – dry• Urine output <1ml/kg/hr• Reduced peripheral temperature

Assessment

Capillary refill

May be useful marker of hypovolemia and myocardial function

Easy but many confounding factors: fever,roomtemp,vasoactive drugs…careful

Core temp vs peripheral temp difference

>3 degrees associated with LCO

Toe Temp -------------

• Hennings et al. -----cardiac index and the normalization of toe temperatures within 6 hours in adults following surgery are associated with good postoperative haemodynamic recovery.

• Knight -----in infants and children after cardiac surgery, toe temperature persistently <32°C even 6 hours after surgery was associated with a poor outcome.

• N. the toe temperature is 1/2way between environmental and core temp

• Toe temperature to environmental temperature gradient is

• less than 2°C poor perfusion state.• Approaches 0.5°C low output state is life

threatening

Assessment • Non-invasive blood pressure monitoring

In patients without edema, values obtained by non-invasive arterial blood pressure monitoring are very close to the values of invasive pressure measurements.

The principal cause of non reliable values with non-invasive pressure measurement is selecting a non-appropriate size of the cuff.

Assessment

• Pulse oximetry

Not accurate with low or very high values (below 80% or with values above 90%-95%)

Be aware of the presence of abnormal hemoglobins

Assessment

• Non Invasive monitoring Chest X-ray

ECG

Urine Output

Chest tube Drainage (Mediastinal Bleeding)

Echocardiography

Assessment

• Invasive monitoring Arterial blood pressure

Central venous pressure

Left atrial pressure

Thermodilution catheters

ABG

Mix venous blood gases

Assessment

• Arterial blood pressure

Hypotension is always pathologic and indicative of dysfunction of the cardiovascular system.

Assessment

2D echo --------very helpful• Quick; non-invasive

• Information

Residual defects

Degree and deviation of shunting

Ventricular function

Systolic

Diastolic

Degree of ventricular filling

Pericardial collections

Normal heart during systole and diastole

LCOS-ECHO

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 inadequate preload ----- Need for volume• High CVP Fluid overload ----------- Diuretic therapy • & Fluid restriction

Diminished RV systolic or diastolic function (in the absence of TV disease or

shunts)• Persistently elevated PAP in relation to systemic BP----

RV dysfunction


Cardiac Output Measurement

Continuous CO measurement to diagnose LCOS with the help of PA catheter, FloTrac, Picco…………………………..best used to interpret trends& to access response to change in therapy, rather than suggest need for intervention because of an abnormal absolute value

Monitoring Of Low CO StateMETABOLIC INDICATORS

LCOS ------- a state of impaired global perfusion anaerobic metabolism and ↑ metabolic acidosis.

Serial ABG analysis reveal ↑ levels of base deficit and ↓HCO3- levels

Frank et al……………….metab acidosis with ↑ pH is a late feature of ↓peripheral perfusion & care takers should not wait for this sign to diagnose LCOS

↑ 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


Mixed Venous Oxygen Tension

• Useful index of circulatory adequacy ……………….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 ………PA catheter or central vein

SVO2 <30 mmHg CO inadequate

SVO2 < 23mmHg severely inadequate CO






How to manage??

MANAGEMENT OF HEMODYNAMIC PROBLEMS

BP PCWP CO SVR Plan

↓ ↓ ↓ ↓ Volume

N ↑ N ↑ Diuretic

↓ ↑ ↓ ↑ Inotrope

↑ ↑ ↓ ↑ Vasodilator

V ↑ ↓ ↑ Ino/vaso/IABP

↓ N N ↓ Alpha-agent

Management------------

Ensure satisfactory oxygenation & ventilation.

Treat ischemia or coronary spasm if suspected to be present --------- -NTG / CCB

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 poorLV function LV function

↓ ↓

15 mmHg Low 20’s(Stiff hypertrophied LV with diastolic

dysfunctionSmall LV Chamber –MS: after LV

resectionPre existing pulm HTN from MV ds)

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-warning

Use of medications with vasodilatation properties like Propofol, narcotics

• 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 abnormalitieshypoxemia

- Systemic venous HTN ↓ Perfusion pressure to other organs.

Kidneys – diuresisGIT – splanchnic congestionBrain – mental state altered

Management of LCOS Heart Rate and Rhythm

Atrio – venticular synchrony with HR of 90-100 b/min------------- 15-20 % improvement in CO provided by atrial contractionAtrial or atrio-ventricular pacing

Reduce Afterload

VasodilatorsMarginal C.O---------------------avoid hypotensionPoor 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)

Management ------------- Maintain blood pressure

Satisfactory C.O. & low SVR ---------- Moderate volume infusion may improve B.P. Commonly seen in sedated patients receiving medications with potent

vasodilator properties.

Marginal C.O.& low SVRNor-epinephrine is preferred (B- agonist prop.; maintenance of peripheral

venous tone ;avoid flooding the pt with volume).

BP & CO Marginal despite multiples ionotropsNorephinephrine

↓

CO still remain low ↓

IABP

Management ----------

If refractory hypotension – vasoplegiaMAP< 50,

Low filling pressures – CVP < 5, PCWP<10

Normal or elevated CI >2.5L/min/m2

Low SVR < 800

VasopressorMethylene blue 1.5 – 2mg/kg – 1 hr

Vasopressin 0.1- 0.4 U/min

Management ------------

Correct Anemia

Blood TransfusionsHct 24%

Difficult to wean from CPB-----/has haemodynamicevidence of severe ventricular dysfunction despite maximal medical therapy and IABP use of circulatory assist devices should be considered

Management ----------

Management---Inotropic and vasoactivedrugs

Selection of drugs

Adequate understanding of underlying cardiac pathophysiology.

Knowledge of α, ß or non adrenergic haemodynamic effects of these drugs.

Inotropic and vasoactive drugs

DOPAMINE1. 2-3 ug/kg/mt ……………………Selective Dopaminergic effect – dilates

renal arteries - ↑ RBF & urine output.2. 3-8 ug/kg/mt……………………..Strong ß1 inotropic effect3. >8 ug/kg/mt ……………………….. Predominant œ effects (direct & by

endogenous NE release) ↑ SVR, ↑ BP, ↑ filling pressures.myocardial O2 consumption ↑

Indications

1st line drug for LCOS especially when SVR is low & BP marginal Profound tachycardia & excessive urine output.


DOBUTAMINE

• Strong ß1 effect : increase contractivity & HR• Mild ß2 effect : ↓ SVR

Indications CO marginal ; Mild elevation in SVR Useful if Dopamine produces profound tachycardia

or excessive urine output.Synergistic effect PDE Inhibitors.



NOREPHINEPHRINE VERSUS DOBUTAMINE in LCOS septic shock

• Difficulty in determining which treatments are most helpful

• Norepinephrine to raising cardiac output in septic shock patients

• EACH PATIENT IS DIFFERENTDellinger RP, Vincent JL. Maintenance of high cardiac output in severe sepsis.

Presented at: 32nd Critical Care Congress; January 30, 2003; San Antonio, Tex.


EPINEPHRINE

Potent ß1 inotropic agent – ↑ CO by ↑ in HR & contractility

<2 ug/mt ß2 effect that produces mild peripheral vasodilatation.

>2 ug/mt, œ effects ↑SVR & ↑ BP with A/E on myocardial O2 metabolism.

Usefulness is limited by the development of tachycardia & arrhythmias


NOREPINEPHRINEPredominant œ effect ↑ SVR & BP ß1 effect ↑ contractility-------------- ↑ myocardial O2

demand & may prove detrimental to ischemic myocardium.

INDICATIONS

Low BP caused by low SVR.

1 - 20µg/mt (0.015-0.2µg/kg/min)


ISOPROTERENOL

Strong ß1 effects but tachycardia limits utilityß2 effects lower SVR, PVR helpful in ↓ Rt. ventricular

after load

INDICATIONS

RV dysfunction with ↑ PVR.

Supplemented by Amrinone / milrinone

0.5 ug/mt -10 ug/mt (0.01- 0.1ug/kg/min)


AMRINONE & MILRINONE

Improve CO by ↓ SVR & PVR and by a moderate + inotropic effect

Indications

Poor CO without initial response to catecholamine or when their use is limited by tachycardia.

RV Dysfunction associated with elevation in PVR


Amrinone : 0.75 mg/kg bolus over 10 mts ------continuous infusion of 10-15 ug/kg/mt

Milrione : 50 ug/kg bolus over 10 mts -----------continuous infusion of 0.375-075 ug/kg/mt


• Mechanisms of a reduced cardiac output and the effects of milrinone and levosimendan in a model of infant cardiopulmonary bypass

Christian F Critical care medicine20-07


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


Tri lodo thyronine (T3)

↑ CO & ↓ SVR in patients with depressed ventricular function.

Randomized studies have not demonstrated a ↓ in inotropicrequirement 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

Vasodilators

• NTG

• SNP

Other drugs

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

N-terminal probrain natriuretic peptide level inversely correlates with cardiac index after arterial switch operation in neonates.Breuer T PaediatrAnaesth. 2007 Aug;17(8):782-8.

http://www.ncbi.nlm.nih.gov/pubmed/17596223?ordinalpos=27&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

Other drugs

• Indications

Diastolic dysfunction

Postcardiotomy systolic dysfunction with elevated PAP

• Dose 2 µg/kg over 1 min followed by 0.01 – 0.03 µg/kg/min

• Rapid onset with peak effect within 30 min, half life 18 min

Other drugs

• Natriuretic Peptides in Septic Patients might eventually prove useful for the diagnosis and/or the treatment of septic patients . Piechota M 2009 current med Chem

Other drugs

Dopexamine• Synthetic catecholamine D as well β2 & less β1

activity

• Inotropic effect by inhibiting neuronal uptake of catecholamines and inc HR dose related

• Dec SVR and improves renal & splanchnic perfusion

• Dec PVR and improves RV function

• Dose 1-4 µg/kg/min

Other drugs

Enoximone• Dec systemic, pulmonary and coronary resistance and

has a positive inotropic activity with minimal effect on HR

• Not associated with thrombocytopenia

• Dose 0.5 -1 mg/kg

• Enoximone in low-output states following cardiac valve replacement was at least equally effective in comparison with standard therapy with epinephrine and nitrolycerin. Werner Zwölfer, Clinical Cardiology,2009

• The Role of Enoximone in the Treatment of Cardiogenic Shock=== Unpredictable.

Other drugs

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

Other drugs

• Corticosteroids…??

• i.v. infusion of methylene blue (0.5 mg/kg)……………..Vasopegic syndrome

Cao Z,Anesth Analg 2009

Intra aortic ballon Pump

• The augmentation of diastolic pressure, to a level higher than systolic pressure, increases coronary perfusion as well as that of other tissues

• Cardiac patients

Indications for Circulatory Assist Devices

Cardiac Surgery

Complete & adequate surgical procedure

Correction of all metabolic problems (ABG, electrolytes)

Inability to wean off bypass despite max pharmalogictherapy & use of IABP

Cardiac Index < 1.8 – 2L/min/m2

Summary and Conclusion

Hypotension is always pathologic and indicative of dysfunction of the cardiovascular system

Do not forget the importance of Toe temperature

Investigations caries some Value

CO may be misleading esp in septic shock

No drug is best

Prevention is better than cure

Mortality can be avoided by timely management in majority of cases

Thank You

Health & Medicine

Low cardiac output syndrome- minati