‘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
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Cool, mottled extremities, poor capillary return
Clouded sensorium
Hypotension
Oliguria
Pulmonary ‘Congestion’
Exclusion of other causes
The Problem
• Definition
– Haemodynamic criteria
• SBP <90mmHg >30min
• CI <2.2L/min m2
• PCWP >15mmHg
Hollenberg, SM. Kavinsky, CJ.
Ann Intern Med. 1999;131:47-59
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
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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 noncatecholamines
• Directly acting agents
– Inotropes
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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
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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 in
limited capacity in trials
• Relatively low mortality
rate
• Significant logistical
challenges
• Typically limited to those
with mechanical causes
of cardiogenic shock
Going Back For Seconds
• Why Treatment Works
– Stunning
– Hibernation
Moving On
• Outcomes
– High mortality
– Limited scope for
recovery