Download management of cardiogenic shock and right heart failure

MANAGEMENT OF CARDIOGENIC SHOCK AND RIGHT HEART FAILURE Siska S. Danny Department of Cardiology and Vascular Medicine Faculty of Medicine Universitas Indonesia NaHonal Cardiovascular Center Harapan Kita Jakarta Indonesia [email protected] CARDIOGENIC SHOCK How to defeat •  Know your enemy •  Treat underlying disease •  Support hemodynamics •  Be fast Cardiogenic Shock: DefiniHon •  Systolic blood pressure <90 mmHg or a value 30 mmHg below basal levels for >30 minutes or catecholamines required to maintain pressure >90 mmHg during systole •  Clinical signs of pulmonary congesHon or pulmonary capillary wedge pressure >15 mmHg •  Signs of impaired organ perfusion (at least 1) – Altered mental status – Cold, clammy skin and extremiHes – Oliguria with urine output <30 mL/h – Serum lactate >2.0 mmol/L •  Arteriovenous oxygen difference >5.5 ml/dL •  Cardiac index <2.2 L/min/m2 Califf RM and Bengtson JR. N Engl J Med 1994; 330:1724-­‐1730 Dry
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•  Syok Kardiogenik • STEMI akut Killip 4 C
European Heart Journal (2012) 33, 1787–1847 TREAT UNDERLYING CAUSE: AMI: CATH à PCI OR CABG OTHERS? IniHal Management of Cardiogenic Shock for AMI Ensure oxygenaHon, intubate and venHlate if necessary Hemodynamic support: fluid challenge, inotropes, vasopressors Intra AorHc Balloon Pump Urgent reperfusion/revascularizaHon European Heart Journal (2012) 33, 1787–1847 Dry
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•  Syok Kardiogenik • STEMI akut Killip 4 C
Diure8k Vasodilator Inotropic drugs : Dobutamine Milrinone Levosimendan Hemodynamic Management •  PA (Swan-­‐Ganz) catheterizaHon à confirm the diagnosis of CS, to ensure that filling pressures are adequate, and to guide changes in therapy à Rarely used nowadays •  Doppler echocardiography à esHmate PA systolic pressure and wedge pressure •  Short mitral deceleraHon Hme (≤140 ms) à highly predicHve of pulmonary capillary wedge pressure ≥ 20 mm Hg in CS Pharmacological Treatment •  Inotropic & vasopressor à use in lowest possible dose •  Inotropes à Increase myocardial ATP consumpHon such that short-­‐term hemodynamic improvement occurs at the cost of increased oxygen demand when the heart is already failing and supply is already limited. Evidence for Use of Inotropes and Vasopressors in Cardiovascular Disease Cardiogenic Shock Complica8ng AMI •  Inotropes and vasopressors à Increase myocardial oxygen consumpHon and can cause ventricular arrhythmias, contracHon band necrosis, and infarct expansion. •  criHcal hypotension à compromises myocardial perfusion à elevated lej ventricular (LV) filling pressures, increased myocardial oxygen requirements, and further reducHon in the coronary perfusion gradient. •  Hemodynamic benefits à outweigh specific risks of inotropic therapy as a bridge to more definiHve treatment •  the lowest possible doses of inotropic and pressor agents should be used to adequately support vital Hssue perfusion while limiHng adverse consequences. •  ACC/AHA for management of hypotension complicaHng AMI –  dobutamine as a first-­‐line agent if systolic blood pressure ranges between 70 and 100 mm Hg in the absence of signs and symptoms of shock. –  Dopamine à in the presence of symptoms of shock. •  If medium dose of dopamine or dopamine/ dobutamine in combinaHon is inadequate, or the paHent’s presenHng systolic blood pressure is < 70 mm Hg, à norepinephrine •  Early shock à endogenous vasopressin levels are elevated significantly to help maintain end-­‐organ perfusion. As shock state progresses àplasma vasopressin levels fall dramaHcally. •  Vasopressin therapy may thus be effecHve in norepinephrine-­‐resistant vasodilatory shock •  Vasopressin à amenuate interleukin-­‐induced generaHon of nitric oxide, have a modest inotropic effect and improve coronary blood flow due to catecholamine sparing. ESC Guidelines on Acute Heart Failure 2005 IniHal Management of Cardiogenic Shock for AMI Ensure oxygenaHon, intubate and venHlate if necessary Hemodynamic support: fluid challenge, inotropes, vasopressors Intra AorHc Balloon Pump Urgent reperfusion/revascularizaHon Basic Principle of IABP •  Helium is rapidly pumped into and out of the balloon. When inflated, this balloon displaces the blood that is in the aorta •  Sudden inflaHon moves blood superiorly and inferiorly to the balloon increasing perfusion to the heart and distal organs (brain, kidneys, Hssues, etc.) à DIASTOLIC AUGMENTATION •  When the balloon is suddenly deflated, the pressure within the aorta drops quickly à AFTERLOAD REDUCTION Hemodynamic effect of a funcHoning IAB CounterpulsaHon INCREASE IN: DECREASE IN: •  Coronary blood flow •  Cardiac output / ejecHon fracHon /
forward flow •  Cerebral and renal blood flow •  Systemic perfusion •  Ajerload à Decreased MVO2 •  LV wall tension •  Preload à Decreased pulmonary congesHon •  Heart Rate PRIMARY EFFECTS OF IABC IAB INfla8on INcreases supply IAB DEfla8on DEcreases demand Cardiogenic Shock: Be Fast AMIS Plus: Treatment of Cardiogenic Shock Jeger RV et al. Ann Intern Med 2008;149:618-­‐626 Right Ventricle •  RV dysfuncHon may cause or contribute to CS. •  CS due to RV dysfuncHon à high RV end-­‐
diastolic pressure, ojen >20 mm à shijing of the interventricular septum toward the LV cavity, à raises lej atrial pressure but impairs LV filling due to the mechanical effect of the septum bowing into the LV à impairs LV systolic funcHon •  Treatment of paHents with RV dysfuncHon and shock à focused on ensuring adequate right-­‐
sided filling pressures to maintain CO and adequate LV preload •  RV end-­‐diastolic pressure of 10 -­‐ 15 mm Hg à associated with higher output •  Inotropic therapy à for RV failure when CS persists ajer RV end-­‐diastolic pressure has been opHmized •  Inhaled nitric oxide (NO) à useful to lower pulmonary vascular resistance and promote forward flow. J Am Coll Cardiol 2010;56:1435–46 Ventricular interdependence
•  During systole, LV protrudes in RV
•  Surrounding pericardium with limited distensibility
•  Compliance of one ventricle can modify the other =
Diastolic ventricular interaction
Vicious cycle of auto-aggravation
Management
•  Control of trigerring factors
•  Supportive treatment:
–  Optimization of preload
–  Improving contractility
–  Pulmonary vasodilators
•  Specific therapies addressing the cause of RVF
Treatment of triggering factors
(acute on chronic)
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Arrhytmias
Infections
Pulmonary embolism
Thyroïd dysfunction
Optimization of preload
Frank-Starling relationship between preload and stroke volume:
preload dependance (A) and preload independance (B)
Fluid therapy
Diuretics
•  Frequent volume overload
•  At a point of Frank-Starling curve where there is
no more reserve on contractility
•  Ventricular interdependance
•  Diuretics to be considered
•  Sometimes with continuous high dose infusion
•  If fails, consider CVVHF
•  Prospective, controlled, randomized, animal study
•  22 dogs underwent transient PA constriction (90mn)
•  Dobutamine 5 and 10 µg/kg/mn, norepinephrine 0.1 to
0.5 µg/kg/mn
•  A transient increase in PA pressure persistently worsens
PA hemodynamics, RV contractility, RV-PA coupling,
and cardiac output.
•  Dobutamine restores RV-PA coupling and cardiac output
better than norepinephrine because of its more
pronounced inotropic effect
Dobutamine
•  β1 adrenergic stimulation
•  ↑ CI ↓ PVR at 5 µg/kg/mn
•  At higher dose ↑ HR without subsequent ↓ in
PVR
•  Experimental models Dobutamine >
Norepinephrine to improve right-ventricular –
pulmonary artery coupling
•  Improves CI, PVR and PaO2/FiO2 in
combination with Inhaled nitric oxyde
Norepinephrine
α1 and β1 adrenergic stimulation
Increases mPAP and PVR
But marked improvement in CO
Useful in combination with Dobutamine for
hypotensive patients
•  Causes less tachycardia than other inotropes
•  Second choice after Dobutamine in
normotensive patients • 
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Addressing the cause of the RV failure, if possible • 
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Treatment of Pulmonary Arterial Hypertension Pericardiotomy/ drainage Thrombolysis / embolectomy Thrombolysis / angioplasty Thromboendarteriectomy Atrial septostomy TransplantaHon CONCLUSION •  CS in modern era: modest decrease of mortality rates due to higher rates of early PCI and IABP use •  IABP sHll a good opHon for early stabilizaHon •  Inotropes and vasopressors should be used judiciously considering the risk and benefit for the paHent •  Newer mechanical hemodynamic support devices are promising but exhibit high complicaHon rates, expensive and limited availability THANK YOU