Cardiogenic Shocksearching for the recent

•Dr. Yasser Ahmed Salem•Lecturer of anesthesia •Ain shams University

Objectives

• Acute right heart syndrome• Takotsubo cardiomyopathy• Pharmacotherapy• Future of heart transplantation• Non pharmacologic therapy

Acute right heart syndrome

• Increase in RV afterload• RV dilates deterioration of

contractility• Right atrial and RV end-diastolic

pressure rise• Cardiac output fall

Contractility:

Power of contraction

Preload:

volume entering ventricles

Afterload:

resistance ventricles must overcome to circulate blood

Precipitating events

• Acute or acute on top of chronic pulmonary embolism

• Deterioration of chronic pulmonary arterial hypertension

• ALI, ARDS or sepsis• Lung resection• LV failure or LV assist device• Cardiac surgery• Heart, lung or liver transplantation

Right Heart Intolerance

CO

AFTERLOAD (MEAN PRESSURE)

RV LV

Positive inotropes

45 mmHg 150 mmHg

Management

Reverse precipitating events

Control contributing factors (acidemia, anemia,

infection, arrhythmia)

Oxygenation and lung protection

Maintain perfusion pressure

Optimize fluid volume

InotropyPulmonary

vasodilators

RV failure

Optimize fluid volume

• Ventricular interdependence

• Cautious fluid administration (bolus and observe response)

• Dilated IVC on echo, unlikely to respond

• Consider cautious diuresis• Massive fluid overload,

consider CVVH

Maintain perfusion pressure

• Norepinephrine, Dopamine, Epinephrine

AIM• To treat systemic hypotension (no

clear winner)• To maintain RV coronary perfusion

without pulmonary vasoconstriction or impaired myocardial performance

Inotropy

Dobutamine (catechol), milrinone (PDE3I)

• Systemic vasodilators

– dobut tachy

– mil decrease BP, often need pressors

• Mild pulmonary vasodilators

• May be used in combination with more potent pulmonary

vasodilators (like inhaled NO or PGI2) to increase CO and

further lower PA pressure

• No clear winner

Bradford et al, J Cardiovasc Pharmacol 2000; 36:146

Pulmonary vasodilators

• Decrease PVR and impedance to reduce RV afterload

• Increase RV stroke volume and cardiac output

• Avoid systemic hypotension and maintain coronary perfusion ( ↓PVR/SVR)

• Avoid hypoxemia (from worsened ventilation/perfusion relationships)

Inhaled prostaglandins

• PGI2 (Prostacyclin)• Potent vasodilator, decrease platelet aggregation• Strong evidence for efficacy in Class IV PAH (improve

functional status and survival)• Given as continuous IV infusion starting at 2 - 4

ng/kg/min, increased as tolerated• Systemic vasodilator, may worsen hypoxemia• Inhaled form is more specific pulmonary vasodilator

• Inhaled ilioprost• given as separate buffs 25 μ gm every 20 min

De Wet et al, J Thorac Cardiovasc Surg 2004; 127: 1061

Kramm et al, Eur J Cardiothor Surg, 2005

Inhaled prostaglandins

Inhaled NO

• Potent vasodilator - stimulates soluble guanylate cyclase in vascular smooth muscle, increase intracellular cGMP

• Usually improves O2 - by enhancing blood flow to ventilated areas

• Virtually no systemic side effects; immediately inactivated by hemoglobin (forms methemoglobin)

• Given by titration in concentrations of 5-40 ppm (little gain > 20 ppm)

limitations

• Withdrawal problems very common (2/3)– Drop SBP, O2 sats, increase PVR– ? Related to suppression of endogenous eNOS

• Methemoglobin and NO2 may accumulate• Very expensive! Up to $3000/day

Phosphodiesterase 5 inhibitors

• Potent acute pulmonary vasodilators by slowing metabolism of cGMP

• Potentiate the effect of iNO or prostacyclin, reduce rebound

• Also systemic vasodilators so must be used with great caution in hypotensive patients

• prelim evidence suggests more selectivity by inhaled routeRuiz M et al, J Heart Lung Txplant 2006

Takotsubo cardiomyopathy

Takotsubo cardiomyopathy

Takotsubo cardiomyopathy

Figure 1. Proposed pathophysiology of takotsubo cardiomyopathy.

Hessel E A , London M J Anesth Analg 2010;110:674-679

Objectives

• Acute right heart syndrome

• Takotsubo cardiomyopathy

• Pharmacotherapy

• Future of heart transplantation

• Non pharmacologic therapy

β-Adreno-receptor Enzyme

SR(Ca++)

ATP

β-Adreno-receptor Enzyme

SR(Ca++)

ATP

cAMP

SR

Ca++

Ca++

Ca++

β-Adreno-receptor Enzyme

SR(Ca++)

ATP

cAMPPDE

PDEI

SR

Ca++

Ca++

Ca++

Clinical Application

  1st Line Agent2nd Line Agent

Septic ShockNorepinephrine (Levophed) Vasopressin

  Phenylephrine (Neosynephrine)

Epinephrine (Adrenalin)

Heart Failure Dopamine Milrinone  Dobutamine Cardiogenic Shock Norepinephrine (Levophed)  Dobutamine Anaphylactic Shock Epinephrine (Adrenalin) Vasopressin

Neurogenic Shock  Phenylephrine (Neosynephrine) 

HypotensionAnesthesia-induced

Phenylephrine (Neosynephrine) 

 Following CABGEpinephrine (Adrenalin)  

Dopexamine

• Newly developed synthetic catecholamine, structurally related to dopamine, dobutamine

• Increase splanchnic(gut, kidney, liver, spleen) blood flow ← stimulation of DA1 receptor

• Increase in stroke volume, heart rate• Decrease in peripheral vascular

resistance ← b2 receptor• Significant increase UO• Inhibitory action in the neuronal

catecholamine uptake mechanism → positive inotropic action

Fenoldopam

• HTN significant and sustained

reduction in blood pressure ( average decrease in diastolic BP 20mmHg)

increased renal blood flow, urine volume sodium excretion, potassium excretion

• CHF dose related increase in CO

by primarily decreasing systemic vascular resistance

no direct inotropic effect

Phosphodiesterase inhibitor

• Bypiridine -amrinone

-milrinone

• Imidazole -enoximone

-piroximone

Phosphodiesterase inhibitor

• Noncatecholamine, nonadrenergic• Inhibition of type III Phophodiesterase ( predominantly in cardiac muscle)

secondary increase in cyclic adenomonophosphatase increase in calcium channel entry into the cell positive inotropic action

• Decrese pulmonary vascular resistance increase cyclic guanidine monophosphate, secondary to incresing NO

from endothelium

• B-agonist additive improvement of myocardial performance

Amrinone

• Treatment of patient with CHF• Perioperative period

positive inotropic and vasodilator action undergoing cardiac surgery

• Augment ventricular performance in vascular surgery pulmonary HTN, chronic pulmonary obstruction in children

Milrinone

• Second generation phosphodiesterase III inhibitor

• Positive inotropic and vasodilating activities 20 times of amrinone increase CO without increasing the overall myocardial oxygen

consumption

• Thrombocytopenia active amrinone metabolite n-acetyl amrinone no reduction in platelet count

Enoximone

• Imidazole PDE inhibitor derivative• CHF awaiting cardiac transplatation,

undergoing CPB• Cardiac and vascular profile

similar to other PDE III inhibitor

• Two potential advantageOral administrationLow incidence of associated dysrhythmia

LEVOSIMENDAN

Dosing

• 6 - 12 µg/kg bolus over 10 min then

• 0.05 – 0.2 µg/kg/min for 24 h

• Correction on hypovolemia

• Correction of potassium and magnesium

• Tight monitoring of blood pressure for 6 h

• Norepinephrine may be added

Future of heart transplant

Dilated Cardiomyopathy

The problem!!!!!!!

Comparison of 1- and 5-year survival after hospitalization for heart failure

Obviously irreversible damage !Obviously irreversible damage !

• More deaths from heart More deaths from heart failure than from any other failure than from any other CV disease CV disease

• 5.3 million symptomatic 5.3 million symptomatic patients; estimated 10 patients; estimated 10 million in 2037million in 2037

• Incidence: About 550,000 Incidence: About 550,000 new cases/yearnew cases/year

• Prevalence is 1% between Prevalence is 1% between the ages of 50 and 59, the ages of 50 and 59, progressively increasing to progressively increasing to >10% over age 80>10% over age 80

American Heart Association. 2008 Heart and Stroke Statistical Update.

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Obviously Big Growing Problem!Obviously Big Growing Problem!

The problem!!!!!!!

• Heart transplantation remains a viable solution for many of these patients

• Shortages in donor supply have limited this valuable resource to <2500 patients per year

• An estimated 10% to 20% of patients die annually on the waiting list

Heart transplantation

SPARITY

Number Of Heart Transplants Number Of Heart Transplants Reported By Year - WorldwideReported By Year - Worldwide

189 317665

1182

2158

2710

31373362

4001 4171 4197 4365 4439 4399 4263 41673833

3563 3410 3367 3269 3180 3026 3095

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500

1000

1500

2000

2500

3000

3500

4000

4500

J Heart Lung Transplant 2007;26: 769-781

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2710

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3563 3410 3367 3269 3180 3026 3095

0

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1000

1500

2000

2500

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3500

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edA plan to treat heart failure by transplantation

?

Have to seek for alternative

Non pharmacologic therapy

Ventricular containment

• ACORN net

• Myosplint

• Skeletal muscle assist

Acorn Cardiac Support Device

Myosplint

Change in radius

R1

R2

Skeletal Muscle Assist

Can Skeletal Muscle Mimic Cardiac Muscle ?

Power Output

Fatigue Resistance

Speed of contraction

Cardiomyoplasty

Cardiomyoplasty What went wrong?

Stimulation Protocol

Fast type converted to slow type

Failure to show systolic improvement

2000 cases worldwide

Medtronic stopped making stimulator

Patients felt better

Minimal survival benefit

Aortomyoplasty

The Biomechanical Heart

Skeletal muscle

ventricle

Girsch, et alSheep model

Skeletal muscle

ventricle

Mechanical assist devices

Principles:1. Direct systolic augmentation of the heart,

2. Mechanical pumping to divert blood from the left atrium/ventricle directly into the aorta with sufficient force to maintain normal arterial pressure,

3. Diastolic augmentation

Mechanical assist devices

• Pulsatile• Heartmate, Jarvik 7

• Axial– Bearings

• Jarvik 2000, Heartmate II

– No Bearings• Heartmate III

Implantable IABP

• The Kantrowitz CardioVADTM (KCV) • 60cc pumping chamber • Percutaneous access device (PAD),• External controller

• Clinical trials• 5 men (age 59 to 73)

Cardiowest artificial heart

It is a pulsatile, pneumaticallydriven prosthetic pair of ventricles made of polyurethane

Cardiowest artificial heart

Cardiowest artificial heart

The Akutsu-III total artificial

heart

The second TAH implanted in a

human.

• survival of medically treated and LVAD patients at 1 year was 48% versus 26%

• and at 2 years was 26% and 8%, respectively.

• Recent modifications of technique and perioperative care have decreased the high LVAD-related morbidity and mortality observed in REMATCH

Park SJ, Tector A, Piccioni W, et al. Left ventricular assist devices as destination therapy: a new look at survival. J Thorac Cardiovasc Surg 2005;129:9 - 17.

REMATCHRandomized Evaluation of Mechanical Assistance Therapy for Congestive Heart Failure

Rose EA, Gelijns AC, Moskowitz AJ, et al. N Engl J Med 2001;345:1435 - 43.

AbioCor Artificial Heart

Cost: $70-100 Grands

Transcuteneus energy transfer

T.E.T.

Pump constituents

Procedure

Procedure improvement

Pulse wave in T.A.H.

•Natural pulse has a 50% diastole time, which gives heart and blood vessels time to relax•Natural pulse has a very steep form