‘cures for a broken heart’
DESCRIPTION
‘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 - PowerPoint PPT PresentationTRANSCRIPT
‘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