Cardiogenic shockCardiogenic shock

นพนพ..รังสฤษฎรังสฤษฎ กาญจนะวณิชยกาญจนะวณิชยคณะแพทยศาสตรคณะแพทยศาสตร มหาวิทยาลัยเชียงใหมมหาวิทยาลัยเชียงใหม

Cardiogenic shock (CS) Cardiogenic shock (CS) AA state of endstate of end--organ hypoperfusion due to cardiacorgan hypoperfusion due to cardiac failurefailure

Evidence of hypoperfusion Evidence of hypoperfusion Cold clammy skin feet/handCold clammy skin feet/handCloudy consciousnessCloudy consciousnessOliguriaOliguria

Systolic BP< 80Systolic BP< 80--90 mmHg90 mmHg-- Persistence after correction of non cardiac factors Persistence after correction of non cardiac factors

Evidence of primary cardiac abnormalityEvidence of primary cardiac abnormalityCardiac index Cardiac index ≤≤ 1.8 L/min/m1.8 L/min/m2 2

LVEDP LVEDP ≥≥ 18 mmHg18 mmHg- adequate or elevated filling pressure

Dry and Dry and WarmWarm

Wet and Wet and WarmWarm

Dry and Dry and ColdCold

Wet and Wet and ColdCold

Fluid statusFluid statusP

erfu

sion

Per

fusi

on

Dry Wet

Warm

Cold

Thai ACS registryThai ACS registry

Mortality according Killip classificationMortality according Killip classification

6.110.2

16.8

49.6

0

10

20

30

40

50

60

I II III IV

%

58%22%

10%

10%

III

III IV

No HF mild HF frank HF Cardiogenic shock

proportionMortality

Cliffhanger

Life on the edge

BP = CO x SVR

BP = ( SV x HR ) x SVR

Stroke volume: ejection fractionpreloadafterload

What causes low What causes low stroke volume?stroke volume?

Causes of Cardiogenic shockCauses of Cardiogenic shockLV /RV pumping failure

ACSFulminant myocarditisAdvanced stage DCMTako-stubo

Valvular abnormalities Severe AS , MSAcute MR , AR

Prosthetic valve thrombosisDynamic LVOT obstruction

Cardiac tamponadeCardiac rupture

Massive pulmonary embolismCardiac shunt (ruptured IVS)Aortic dissection

Acute severe AR

Risk factors for development of CS in ACSRisk factors for development of CS in ACS

Older ageAnterior wall MIHTDMMultivessel CADPrior MIHx of HFSTEMILBBB

Myocardial dysfunction

Myocardial ischemia

Poor coronary perfusion

hypotension

Progressive myocardial dysfunction

death

PathophysiologyPathophysiology

Management of cardiogenic shockManagement of cardiogenic shock

Identify causeIdentify causeRhythmRhythmLow stroke volumeLow stroke volume

Physical signsPhysical signsEchocardiogramEchocardiogramInvasive hemodynamic monitoringInvasive hemodynamic monitoring

EchocardiographyEchocardiography

Severe LV systolic dysfunction

Triads of RV infarctionTriads of RV infarction

HypotensionElevated JVPClear lung fields

RV dilatation and impaired RV systolic function

Ruptured ventricular septumRuptured ventricular septum

Large defectLarge defect

PitfallPitfall

LV

LA

RV

RA

Watershed area

Ruptured septumRuptured septum

Acute infero-posterior wall MI with ruptured PM papillary muscle

Ruptured papillary muscleRuptured papillary muscle

Ruptured papillary muscleRuptured papillary muscle

Chronic MR acute MR

Clinical profile of complications of AMIClinical profile of complications of AMI

VSDVSD Papillary muscle rupturePapillary muscle rupture

SymptomsSymptoms May be less severeMay be less severe Severe pulmonary edemaSevere pulmonary edema

Infarct siteInfarct site AnteriorAnterior Posterior / InferiorPosterior / Inferior

New murmurNew murmur AlwaysAlways Usually but can be soft or Usually but can be soft or absentabsent

ThrillThrill YesYes Uncommon Uncommon

PA catheterPA catheter OO22 step up in RVstep up in RV Prominent CV wave in Prominent CV wave in PCWP tracingPCWP tracing

AMI with shock and pulmonary

edema with good LVEF

Think of ruptured IVS , papillary

muscle

Free wall ruptureFree wall rupture

Free wall rupture and Free wall rupture and hemopericardiumhemopericardium

General Support MeasuresGeneral Support MeasuresASAEnoxaparinDefer Clopidrogrel until after coronary angiography (emergent CABG may be needed)Negative inotropes and vasodilators (including nitroglycerin) should be avoidedArterial oxygenation and near-normal pH should be maintainedIntensive insulin therapyLow threshold to institute mechanical ventilation via mask (BiPAP) or endotracheal tube

Management of cardiogenic shockManagement of cardiogenic shock

• Optimize LV filling pressure

• Inotropic and vasopressor agents

• Early intraaortic ballon pump

• Prompt revascularization

Optimize LV filling pressureOptimize LV filling pressure

To Swan or not to STo Swan or not to Sw

of PAC

E / E’early diastolic LA-LV

pressure gradient

LAP and LV suction

early diastolic myocardial relaxation

velocity

Normal heartincreasing transmitral gradient, preload exercise increased both E and E’

Myocardial diseaseincreasing transmitral gradient, preload exercise increased E but E’ remains low

Echo derived E/EEcho derived E/E’’““non invasive Swannon invasive Swan--GanzGanz””

LVEDP > 18 mmHg

Comparison of Hemodynamics in ShockComparison of Hemodynamics in Shock

Parameter Hypovolemic Cardiogenic Neurogenic Anaphylactic Early septic Late septic

CVP ↓ ↑ ↓ ↓ ↓ ↓PAWP ↓ ↑ ↓ ↓ ↓ or = ↑

CO ↓ ↓ ↓ ↓ ↑ ↓BP ↓ ↓ ↓ ↓ ↓ or = ↓

SVR ↑ ↑ ↓ ↓ ↓ ↑HR ↑ ↑ ↓ ↑ = ↑

Fluid management in MI with AHF Fluid management in MI with AHF ‐‐ PitfallsPitfalls

• Redistribution of intravascular volume into the lungs leads to a net acute decrease in circulating plasma volume in those without prior chronic heart failure.

• When high-dose diuretics are administered, plasma volume declines further

• A trial of a low diuretic dose coupled with low-dose nitrates and positional measures to decrease preload (eg, seated position with legs down) should be attempted in patients with MI and pulmonary edema to avoid precipitating shock.

RV infarction

• The common practice of aggressive fluid resuscitation for RV dysfunction in shock may be misguided.

• Excess volume loading in patients with RV infarction may cause or contribute to shock.

• The elevation of RV end-diastolic pressure may result in shifting of the interventricular septum toward the LV cavity, which impairs LV filling due to the mechanical effect of the septum bowing into the LV

RV

LV

Inotropic agents/vasopressorsInotropic agents/vasopressors

• Dopamine– <2 renal vascular dilation

– <2‐10 +chronotropic/inotropic (beta effects)

– >10 vasoconstriction (alpha effects)

• Dobutamine (Dobutrex®)– positive inotrope, vasodilates, arrhythmogenic at higher doses

• Norepinephrine (Levophed®)

– vasoconstriction, inotropic stimulant. Should only be used for refractory hypotension with low SVR.

• Norepinephrine should only be used as a last resort

Inotropic and vasopressor agentsInotropic and vasopressor agents

• Use at lowest possible doses

• Increased myocardial ATP consumption

• Direct toxic effect

• May induce AF / ventricular arrhythmias

• Short term hemodynamic improvement occurs at the cost of increased O2 demand

Vasopressors do not change outcome and Vasopressors do not change outcome and is is notnot the definite therapythe definite therapy

Management of cardiogenic shockManagement of cardiogenic shock

• Optimize LV filling pressure

• Inotropic agents

(Dopamine, Dobutamine)

• Early intraaortic ballon pump

• Prompt revascularization

Diastole: Inflation

Augmentation of diastolic pressure

Increased coronary perfusion

Systole: deflationcreates a vacuum effect

decreased afterloadDecreased cardiac workDecreased myocardial oxygen consumptionIncreased cardiac output

Indication for IABPIndication for IABP

Cardiogenic shock not quickly reversed with

pharmacologic therapy as a stabilizing measure for angiography and prompt

revascularization

Time = Muscle

Prompt RevascularizationPrompt Revascularization

Fibrinoloytic1o PCI

Benefit of early revascularizationBenefit of early revascularization

SHOCK trial N Engl J Med 1999;341: 625-634.

Survival benefit in < 48 hrs after MI, < 18 hrs after shock onset

In patient less than 75 years of age : 6 months mortality 44.9% VS 65%

ARR = 20% NNT = 5 !

Efficient referral system

Rapid consultation / activation of

Northern ACS NetworkNorthern ACS Network

Centre with cardiologist

Centre with Cath Lab

Centre with 24 hrs 1oPCI

Fibrinolysis Centre without Cardiologist

คําแนะนําสําหรบัการสงตอคําแนะนําสําหรบัการสงตอ cardiogenic shockcardiogenic shock

• เตรียมผูปวยใหพรอม โดยการทําการรักษาเบื้องตนใหถึงขั้นที่ปลอดภัยเพียงพอที่จะสงตอไปยังโรงพยาบาลปลายทางได

• ประสานงานกับโรงพยาบาลที่รับผูปวย – การเตรียมของโรงพยาบาลปลายทางเปนสิง่ทีท่ําใหผูปวยมีโอกาสรอดชีวิตไดเพิ่มขึ้น

• เตรียมอุปกรณที่จําเปนไปกับรถพยาบาล IABP ECG monitor AED• ACLS competent personnel• มีแพทยเดินทางไปดวย• อธิบายใหญาติผูปวยยอมรับความเสี่ยงที่อาจเกิดขึ้นในระหวางการเดินทางกอนทุก

ครั้ง

Centralized careCentralized care

TCTC

Networking and decentralizationNetworking and decentralization

PCPC

PCPC PCPC

PCPC

PCPC

TCTC

PC : Primary careTC : Tertiary care

How to manage cardiogenic shock in How to manage cardiogenic shock in hospitals without revascularization hospitals without revascularization

capability ?capability ?

A strategy of early fibrinolysis and IABP followed by immediate transfer for PCI or CABG may be appropriate.

Sanborn et al, JACC 2000;361123‐29

Time sensitive reperfusion strategies Time sensitive reperfusion strategies

No benefit of revascularizationNo benefit of revascularization

• Prolonged shock

• Multiple organ failure

• Anoxic brain damage

Do not transfer these patients

Be aheadBe ahead

Dynamic Do not wait for an overt indication before starting a therapy.Once SIR develops,

it’s almost always too late.Early IABPEarly transfer

Prompt diagnosis Prompt diagnosis Prompt treatment Prompt treatment

If all fail …..