Download Cardiogenic Shock searching for the recent

Cardiogenic Shock
searching 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
Preload:
Afterload:
volume
entering
ventricles
resistance
ventricles must
overcome to
circulate blood
Contractility:
Power of
contraction
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
Positive inotropes
CO
RV
45 mmHg
AFTERLOAD (MEAN PRESSURE)
LV
150 mmHg
Management
Reverse
precipitating events
Maintain perfusion
pressure
Control contributing
factors (acidemia, anemia,
infection, arrhythmia)
RV failure
Optimize fluid
volume
Oxygenation and
lung protection
Inotropy
Pulmonary
vasodilators
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
De Wet et al, J Thorac Cardiovasc Surg 2004; 127: 1061
• Inhaled ilioprost
• given as separate buffs 25 μ gm every 20 min
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 route
Ruiz 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
ATP
β-Adrenoreceptor
Enzyme
SR
(Ca++)
ATP
β-Adrenoreceptor
Enzyme
Ca++
Ca++
Ca++
cAMP
SR
(Ca++)
ATP
β-Adrenoreceptor
Enzyme
Ca++
Ca++
Ca++
PDE
PDEI
cAMP
SR
SR
(Ca++)
Clinical Application
Septic Shock
Heart Failure
Cardiogenic
Shock
1st Line Agent
2nd Line Agent
Norepinephrine (Levophed)
Phenylephrine
(Neosynephrine)
Dopamine
Dobutamine
Vasopressin
Epinephrine
(Adrenalin)
Milrinone
Norepinephrine (Levophed)
Dobutamine
Anaphylactic
Shock
Epinephrine (Adrenalin)
Phenylephrine
(Neosynephrine)
Neurogenic Shock
Anesthesia- Phenylephrine
(Neosynephrine)
Hypotension
induced
Following
CABG
Epinephrine (Adrenalin)
Vasopressin
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 advantage
Oral administration
Low 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
The problem!!!!!!!
Comparison of 1- and 5-year survival after hospitalization for
heart failure
Obviously irreversible damage !
Dilated Cardiomyopathy
The problem!!!!!!!
Heart Failure Patients in US
(Millions)
12
10
10
• More deaths from heart
failure than from any other
CV disease
• 5.3 million symptomatic
patients; estimated 10
million in 2037
8
5.3
Obviously
Big Growing Problem!
6
4
• Incidence: About 550,000
new cases/year
3.5
2
0
1991
2005
2037*
• Prevalence is 1% between
the ages of 50 and 59,
progressively increasing to
>10% over age 80
American Heart Association. 2008 Heart and Stroke Statistical Update.
Heart transplantation
• Heart transplantation remains a viable solution
for many of these patients
SPARITY
• 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
Number Of Heart Transplants
Reported By Year - Worldwide
J Heart Lung Transplant 2007;26: 769-781
A plan10to treat heart failure by
transplantation
10
Heart Transplants Performed
Heart Failure Patients in US
(Millions)
12
8
5.3
6
4
3.5
2
0
1991
2005
2037*
?
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 al
Sheep 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,
pneumatically
driven 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 .
REMATCH
Randomized 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.
• 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.
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