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1
Cures For A Broken Heart
  • Cardiogenic Shock, IABP, Vasopressors, Inotropes
    Cardiologists
  • Daniel Orr

2
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

3
The Problem
  • Definition
  • Haemodynamic criteria
  • SBP lt90mmHg gt30min
  • CI lt2.2L/min m2
  • PCWP gt15mmHg

4
The Problem
  • Incidence
  • Range 5 10 patients presenting with AMI
  • Does not account for out of hospital arrests/death

5
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

6
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

7
The Breakdown
  • Pathophysiology
  • Described as a downward spiral of events of
    compounding events
  • Key Elements
  • Primary Pump Failure
  • Sympathetic Nervous System Activation

8
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

9
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

10
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

11
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

12
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

13
Damage Control
  • Initial Management
  • General Supportive
  • Infarct
  • Shock

14
Damage Control
  • Initial Management
  • General Supportive
  • Correct hypoxia / acidosis
  • Relieve pain
  • Correct electrolytes

15
Damage Control
  • Initial Management
  • Infarct
  • Aspirin
  • Clopidogrel
  • Heparin
  • GPIIb/IIIa inhibitors
  • NSTEMI

16
Damage Control
  • Initial Management
  • Infarct
  • Thrombolysis / PTCA / CABG / VR
  • Avoidance of agents with negative inotropic
    effects - beta blockers, calcium channel blockers

17
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

18
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

19
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

20
Putting The Squeeze On
  • First Line
  • Dopamine
  • Noradrenaline
  • Second Line
  • Dobutamine
  • Milrinone

21
Putting The Squeeze On
  • First Line
  • Dopamine
  • Naturally occuring sympathomimetic amine, with
    effects at a, ß, and DA receptors
  • Low dose ß effects predominate, high does a
  • Both vasoconstrictor and inotropic effects
  • Increases PCWP
  • Risk of arrhythmia (gtNA latest NEJM)
  • Tachycardia, increased O2 demand

22
Putting The Squeeze On
  • First Line
  • Noradrenaline
  • Potent naturally occurring sympathomimetic amine
    and neurotransmitter, with effects at a ß
    receptors
  • Predominant a effects
  • Tissue necrosis
  • Risk of arrhythmia
  • Adrenaline - substitute for Dopamine

23
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

24
Putting The Squeeze On
  • Second Line
  • Dobutamine
  • Synthetic catecholamine, predominantly ß effects
  • Increases inotropy and chronotropy, often of
    benefit in cardiac failure
  • May worsen hypotension
  • Risk of arrhythmia
  • Can be combined with Dopamine

25
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

26
Party Time
  • IABP other VADs
  • Benefit of improving coronary perfusion and
    cardiac performance
  • Reduce myocardial ischaemia cardiac work
  • Do not alter SVR

27
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

28
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29
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

30
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

31
Party Time
  • IABP
  • Contraindications
  • Absolute
  • Moderate Severe Aortic Regurgitation
  • Dissecting Aortic Aneurysm
  • Relative
  • PVD
  • AAA

32
Party Time
  • IABP
  • Complications
  • Vascular
  • Limb ischaemia
  • Vascular laceration
  • Major Haemorrhage
  • Non-Vascular
  • Embolization
  • Balloon migration ischaemia cerebral, renal
  • Sepsis
  • Balloon rupture

33
Party Time
  • IABP
  • Complications
  • Other
  • Haemolysis
  • Thrombocytopaenia
  • Peripheral neuropathy
  • Practical
  • Anticoagulation
  • Post CABG
  • AMI

34
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

35
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36
Party Time
  • IABP
  • Practical
  • Modes - 11, 12, 14
  • 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 14

37
Finding Solutions
  • Definitive Treatment
  • Thrombolysis
  • Revascularization
  • CABG / VR

38
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

39
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

40
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

41
Going Back For Seconds
  • Why Treatment Works
  • Stunning
  • Hibernation

42
Moving On
  • Outcomes
  • High mortality
  • Limited scope forrecovery
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