Cardiogenic Shock searching for the recent
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Transcript of Cardiogenic Shock searching for the recent
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Cardiogenic Shocksearching for the recent
•Dr. Yasser Ahmed Salem•Lecturer of anesthesia •Ain shams University
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Objectives
• Acute right heart syndrome• Takotsubo cardiomyopathy• Pharmacotherapy• Future of heart transplantation• Non pharmacologic therapy
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Acute right heart syndrome
• Increase in RV afterload• RV dilates deterioration of
contractility• Right atrial and RV end-diastolic
pressure rise• Cardiac output fall
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Contractility:
Power of contraction
Preload:
volume entering ventricles
Afterload:
resistance ventricles must overcome to circulate blood
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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
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Right Heart Intolerance
CO
AFTERLOAD (MEAN PRESSURE)
RV LV
Positive inotropes
45 mmHg 150 mmHg
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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
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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
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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
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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
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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)
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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
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Inhaled prostaglandins
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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)
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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
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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
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Takotsubo cardiomyopathy
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Takotsubo cardiomyopathy
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Takotsubo cardiomyopathy
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Figure 1. Proposed pathophysiology of takotsubo cardiomyopathy.
Hessel E A , London M J Anesth Analg 2010;110:674-679
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Objectives
• Acute right heart syndrome
• Takotsubo cardiomyopathy
• Pharmacotherapy
• Future of heart transplantation
• Non pharmacologic therapy
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β-Adreno-receptor Enzyme
SR(Ca++)
ATP
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β-Adreno-receptor Enzyme
SR(Ca++)
ATP
cAMP
SR
Ca++
Ca++
Ca++
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β-Adreno-receptor Enzyme
SR(Ca++)
ATP
cAMPPDE
PDEI
SR
Ca++
Ca++
Ca++
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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)
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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
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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
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Phosphodiesterase inhibitor
• Bypiridine -amrinone
-milrinone
• Imidazole -enoximone
-piroximone
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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
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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
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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
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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
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LEVOSIMENDAN
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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
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Future of heart transplant
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Dilated Cardiomyopathy
The problem!!!!!!!
Comparison of 1- and 5-year survival after hospitalization for heart failure
Obviously irreversible damage !Obviously irreversible damage !
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• 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.
3.5
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Obviously Big Growing Problem!Obviously Big Growing Problem!
The problem!!!!!!!
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• 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
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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
0
500
1000
1500
2000
2500
3000
3500
4000
4500
J Heart Lung Transplant 2007;26: 769-781
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3.5
5.3
10
0
2
4
6
8
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1991 2005 2037*
Hea
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ailu
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atie
nts
in
US
(Mil
lio
ns)
2710
3137
4171 4197 4365 4439 4399 4263 41673833
3563 3410 3367 3269 3180 3026 3095
0
500
1000
1500
2000
2500
3000
3500
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Hea
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Per
form
edA plan to treat heart failure by transplantation
?
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Have to seek for alternative
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Non pharmacologic therapy
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Ventricular containment
• ACORN net
• Myosplint
• Skeletal muscle assist
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Acorn Cardiac Support Device
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Myosplint
Change in radius
R1
R2
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Skeletal Muscle Assist
Can Skeletal Muscle Mimic Cardiac Muscle ?
Power Output
Fatigue Resistance
Speed of contraction
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Cardiomyoplasty
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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
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Aortomyoplasty
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The Biomechanical Heart
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Skeletal muscle
ventricle
Girsch, et alSheep model
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Skeletal muscle
ventricle
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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
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Mechanical assist devices
• Pulsatile• Heartmate, Jarvik 7
• Axial– Bearings
• Jarvik 2000, Heartmate II
– No Bearings• Heartmate III
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Implantable IABP
• The Kantrowitz CardioVADTM (KCV) • 60cc pumping chamber • Percutaneous access device (PAD),• External controller
• Clinical trials• 5 men (age 59 to 73)
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Cardiowest artificial heart
It is a pulsatile, pneumaticallydriven prosthetic pair of ventricles made of polyurethane
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Cardiowest artificial heart
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Cardiowest artificial heart
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The Akutsu-III total artificial
heart
The second TAH implanted in a
human.
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• 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.
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AbioCor Artificial Heart
Cost: $70-100 Grands
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Transcuteneus energy transfer
T.E.T.
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Pump constituents
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Procedure
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Procedure improvement
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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
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