‘Cures For A Broken Heart’

• Cardiogenic Shock, IABP, Vasopressors, Inotropes & Cardiologists

Daniel Orr

The Problem

• Definition• ‘Decreased cardiac output and evidence of tissue

hypoxia in the presence of adequate intravascular volume.’

– Clinically• Cool, mottled extremities, poor capillary return• Clouded sensorium• Hypotension• Oliguria• Pulmonary ‘Congestion’• Exclusion of other causes

Hollenberg, SM. Kavinsky, CJ. Ann Intern Med. 1999;131:47-59

The Problem

• Definition

– Haemodynamic criteria• SBP <90mmHg >30min• CI <2.2L/min m2

• PCWP >15mmHg

The Problem

• Incidence

– Range 5 – 10% patients presenting with AMI

– Does not account for out of hospital arrests/death

The Trigger

• Cause & Epidemiology– Myocardial Infarct

• Majority of cases – Pump failure• Include right ventricular infarct

– Mechanical Events• Acute MR• Rupture IVS or free wall

– Myocardial Dysfunction• Myocarditis, Cardiomyopathy, Septic Shock, Prolonged

CPB

Risk Factors & Evolution

• Shock• More likely in those with anterior and previous

infarct, old, the diabetic, PVD, CVA

• Time Course• Of those reaching hospital minority of patients in

shock ~ 10%• 7 hours typical delay between infarct and

symptomatic shock

The Breakdown

• Pathophysiology– Described as a downward spiral of events of

compounding events

– Key Elements

• Primary Pump Failure

• Sympathetic Nervous System Activation

The Breakdown

• Pathophysiology– Pump Failure

• Both systolic & diastolic components

• Systolic– Reduction in stroke volume, therefore cardiac output– Remainder of myocardium hypercontractile, increasing

O2 consumption

– Significant dependence on coronary flow, potentially already compromised by disease

– All worsen ischaemia

The Breakdown

• Pathophysiology– Pump Failure

• Diastolic– Perfusion reduced by hypotension and SNS induced

tachycardia– Increased EDP additionally reduces perfusion

– Increased wall stress increases O2 consumption

– All worsen ischaemia

The Fallout

• Pathophysiology– Sympathetic Activation

• Attempt to maintain organ perfusion

• Results– Tachycardia– Increased circulating catecholamines– Activation of RAA system

• Consequences– Increased myocardial O2 demand via HR, contractility,

afterload – Increased preload via RAA– Worsening ischaemia & Pulmonary consequences

The Fallout

• Pathophysiology– Tissue Hypoxia

• Results in increased products of anaerobic metabolism including lactate, and a decrease in pH

• Worsens myocardial performance

– The Latest• Systemic inflammatory response• Cytokines, interleukins, inducible NO synthase• Consequences for genesis, treatment & outcome

Assessing The Damage

• Symptoms & Signs• Emergency - ‘Time is muscle’ (or Tissue)

• Signs of inadequate tissue perfusion

• CVS including elevated JVP, pulmonary oedema, extra heart sounds, murmur, arrhythmia

• Echo - wall motion, papillary muscle, valvular function

• Invasive monitoring

Damage Control

• Initial Management– General Supportive

– Infarct

– Shock

Damage Control

• Initial Management– General Supportive

• Correct hypoxia / acidosis

• Relieve pain

• Correct electrolytes

Damage Control

• Initial Management– Infarct

• Aspirin• Clopidogrel• Heparin• GPIIb/IIIa inhibitors

– NSTEMI

Damage Control

• Initial Management– Infarct

• Thrombolysis / PTCA / CABG / VR

• Avoidance of agents with negative inotropic effects - beta blockers, calcium channel blockers

Damage Control

• Initial Management– Shock

• Volume resuscitation, especially if cause is due to RV infarction

– Guided by Sats, MAP, CO, PCWP - aim for lowest value to give highest CO. Often 18-25mmHg

– Pulmonary oedema• Diuretics• Vasodilators

Invasive monitoring

• All modalities should be considered• Arterial line - almost universal

• Central line - required for administration of inotropes

• PA catheter / PiCCO– Refractory hypotension– Mechanical complications & cause– Vasopressor / Inotropic agents

Putting The Squeeze On

• Vasopressors & Inotropes– Vasopressors

• Agents that produce vasoconstriction

• Mostly sympathomimetics, catechol and non-catecholamines

• Directly acting agents

– Inotropes• Agents that increase myocardial contractility

• Sympathomimetics

• Phosphodiesterase inhibitors

• Others

Putting The Squeeze On

• First Line– Dopamine– Noradrenaline

• Second Line– Dobutamine– Milrinone

Putting The Squeeze On

• First Line– Dopamine

• Naturally occuring sympathomimetic amine, with effects at α, β, and DA receptors

• Low dose β effects predominate, high does α• Both vasoconstrictor and inotropic effects

• Increases PCWP• Risk of arrhythmia (>NA latest NEJM)

• Tachycardia, increased O2 demand

Putting The Squeeze On

• First Line– Noradrenaline

• Potent naturally occurring sympathomimetic amine and neurotransmitter, with effects at α & β receptors

• Predominant α effects

• Tissue necrosis• Risk of arrhythmia

– Adrenaline - substitute for Dopamine

Putting The Squeeze On

• First Line– Considerations

• Vasopressors typically increase SVR, with limited direct effect on CO

• Increased SVR may worsen CO - consider invasive monitoring

Putting The Squeeze On

• Second Line– Dobutamine

• Synthetic catecholamine, predominantly β effects• Increases inotropy and chronotropy, often of

benefit in cardiac failure

• May worsen hypotension• Risk of arrhythmia• Can be combined with Dopamine

Putting The Squeeze On

• Second Line– Milrinone

• Selective PDE III inhibitor inotropic agent• Increases CO via increased cAMP• Additionally has vascular vasodilating effects

• Risk of hypotension and arrhythmia• No studies to demonstrate benefit

Party Time

• IABP & other VADs– Benefit of improving coronary perfusion and

cardiac performance

– Reduce myocardial ischaemia & cardiac work

– Do not alter SVR

Party Time

• IABP– Description

• Intravascular counterpulsation device used to augment cardiac function

– Haemodynamic Effects• Displacement of blood into proximal aortic territory

during diastole– Increases coronary & cerebral blood flow

• Reduction in afterload 2o to ‘vacuum’ effect– Reduces cardiac work

Party Time

• IABP– Consequences

• Improved myocardial O2 supply and reduced O2 demand

• Improvement in end organ function, reduction in acidosis

• In cardiogenic shock used as adjunct to definitive treatment. In isolation does not improve mortality

Party Time

• IABP– Uses/Indications

• Cardiogenic shock– Including AMI & mechanical lesions eg MR

• Support post PTCA• Weaning from CPB• Refractory unstable angina / High risk restenosis

PTCA or thrombolysis

Party Time

• IABP– Contraindications

• Absolute– Moderate & Severe Aortic Regurgitation– Dissecting Aortic Aneurysm

• Relative– PVD– AAA

Party Time

• IABP– Complications

• Vascular– Limb ischaemia– Vascular laceration– Major Haemorrhage

• Non-Vascular– Embolization– Balloon migration & ischaemia cerebral, renal– Sepsis– Balloon rupture

Party Time

• IABP– Complications

• Other– Haemolysis– Thrombocytopaenia– Peripheral neuropathy

– Practical• Anticoagulation

– Post CABG– AMI

Party Time

• IABP– Practical

• Triggering– ECG– Pacing– Arterial pressure

• Monitoring– Peak diastolic will be higher than systolic (augmented)– Continue to use MAP on IBP to guide ‘tropes’

Party Time

• IABP– Practical

• Modes - 1:1, 1:2, 1:4

• Size does matter– Differing volume of balloon for height

• Weaning– Stable haemodynamics typically after 24-48/24– Reduce inflation ratio, off after ~ 2/24 at 1:4

Finding Solutions

• Definitive Treatment– Thrombolysis

– Revascularization

– CABG / VR

Finding Solutions

• Definitive Treatment– Thrombolysis

• Evidence suggests benefit over placebo in cardiogenic shock, improved survival

• Use in combination with IABP

• PTCA and CABG superior

• Consider in patients who are high risk, in areas without angiographic services

Finding Solutions

• Definitive Treatment– Revascularization

• Mainstay of AMI induced cardiogenic shock• Early intervention preferable• Improvement in both infarct and remote

myocardium

• Response may be variable, and not immediately apparent

Finding Solutions

• Definitive Treatment– CABG / VR

• Benefit demonstrated inlimited capacity in trials

• Relatively low mortalityrate

• Significant logisticalchallenges

• Typically limited to thosewith mechanical causesof cardiogenic shock

Going Back For Seconds

• Why Treatment Works– Stunning

– Hibernation

Moving On

• Outcomes– High mortality

– Limited scope forrecovery