Sandbox: Cardiogenic Shock

Template:Cardiogenic Shock - 2017 Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1],Associate Editor(s)-in-Chief: Arzu Kalayci, M.D. [2]

Contemporary Management of Cariogenic Shock

Pragmatic and Clinical Trial Definitions of Cardiogenic Shock

Clinical Definition	SHOCK Trial	IABP-SHOCK II	ESC HF Guidelines
Cardiac disorder that results in both clinical and biochemical evidence of tissue hypoperfusion	Clinical criteria: SBP <90 mmHg for ≥30 min OR Support to maintain SBP ≥90 mmHg AND End-organ hypoperfusion (urine output <30 mL/h or cool extremities) Hemodynamic criteria: CI of ≤2.2 L·min−1·m−2 AND PCWP ≥15 mmHg	Clinical criteria: SBP <90 mmHg for ≥30 min OR Catecholamines to maintain SBP >90 mmHg AND Clinical pulmonary congestion AND Impaired end-organ perfusion (altered mental status, cold/clammy skin and extremities, urine output <30 mL/h, or lactate >2.0 mmol/L)	SBP <90 mmHg with adequate volume and clinical or laboratory signs of hypoperfusion Clinical hypoperfusion: Cold extremities, oliguria, mental confusion, dizziness, narrow pulse pressure Laboratory hypoperfusion: Metabolic acidosis, elevated serum lactate, elevated serum creatinine
CI indicates cardiac index; CS, cardiogenic shock; ESC, European Society of Cardiology; HF, heart failure; IABP-SHOCK II, Intraaortic Balloon Pump in Cardiogenic Shock II; LV, left ventricular; MI, myocardial infarction; PCWP, pulmonary capillary wedge pressure; SBP, systolic blood pressure; and SHOCK, Should We Emergently Revascularize Occluded Coronaries for Cariogenic Shock

Potential Hemodynamic Presentations of Cardiogenic Shock

Volume Status
Peripheral Circulation	Cold	Classic Cardiogenic Shock or Mixed Shock (↓Cl; ↑SVRI; ↑PCWP)	Euvolemic Cardiogenic Shock (↓Cl; ↑SVRI;↔PCWP)
	Warm	Vasodilatory Cardiogenic Shock or Mixed Shock (↓Cl; ↓/↔SVRI;↑PCWP)	Vasodilatory Shock (Not Cardiogenic Shock) (↑Cl; ↓SVRI; ↓PCWP)
CI indicates cardiac index; PCWP, pulmonary capillary wedge pressure; and SVRI, systemic vascular resistance index.

Considerations for Initial Critical Care Monitoring in Patients With Cardiogenic Shock

Monitoring Parameter	Frequency	Comment/Rationale
Noninvasive Monitoring
Telemetry, pulse oximetry, respiratory rate	Continuous	High incidence of arrhythmias, ventilator failure, and pulmonary edema
Critical care unit monitoring	1:1 Nurse-to-patient ratio	High incidence of hemodynamic deterioration and multisystem organ failure
Invasive monitoring
Arterial BP monitoring	Continuous	Consider continuing until vasoactive medications have been discontinued for 12–24 h
CVP	Continuous	A central line is required for delivery of vasoactive medications; single-point-in-time CVP measurements may be unreliable measures of uid status, but longitudinal CVP trends may provide information on trends in fluid status
Central venous oxygen saturation	Every 4 h	Trends in central venous oxygen saturation in patients with a central line can be used to help monitor trends in cardiac output
Urine output	Every hour	Urine output and serum creatinine monitoring are markers of renal perfusion and acute kidney injury
PAC or noninvasive cardiac output monitor	Selected use	Consider using early in the treatment course in patients not responsive to initial therapy or in cases of diagnostic or therapeutic uncertainty
Laboratory Investigations
Complete blood counts	Every 12–24 h	Consider more frequently in patients with CS with, or at high risk for, bleeding
Serum electrolytes	Every 6–12 h	Frequency should be tailored to risks or presence of renal failure and electrolyte dycrasias
Serum creatinine	Every 12–24 h	Urine output and serum creatinine monitoring are markers of renal perfusion and acute kidney injury
Liver function tests	Daily	Monitoring for congestive hepatopathy and hypo perfusion
Lactate	Every 1–4 h	Lactate clearance is a marker of resolving end-organ hypoperfusion, and lack of clearance is associated with a higher risk of mortality
Coagulation laboratories	Every 4–6 h for those on anticoagulants until therapeutically stable, every 24 h if patient is not on anticoagulants	Altered drug elimination and frequent use of mechanical support devices often necessitate antithrombotic monitoring
BP indicates blood pressure; CS, cardiogenic shock; CVP, central venous pressure; and PAC, pulmonary artery catheter.

Mechanism of Action and Hemodynamic Effects of Common Vasoactive Medications in Cardiogenic Shock

Clinical Definition	SHOCK Trial	IABP-SHOCK II	ESC HF Guidelines	SHOCK Trial	IABP-SHOCK II	ESC HF Guidelines
		Receptor Binding
Medication	Usual Infusion Dose	α1	β1	β2	Dopamine	Hemodynamic Effects
Vasopressor / Inotropes
Dopamine	0.5–2 μg·kg-¹·min-¹	−	+	−	+++	↑CO
	5–10 μg·kg-¹·min-¹	+	+++	+	++	↑↑CO, ↑SVR
	10–20 μg·kg-¹·min-¹	+++	++	−	++	↑↑SVR, ↑CO
Norepinephrine	0.05–0.4 μg·kg-¹·min-¹	++++	++	+	−	↑↑SVR, ↑CO
Epinephrine	0.01–0.5 μg·kg-¹·min-¹	++++	++++	+++	−	↑↑CO, ↑↑SVR
Phenylephrine	0.1–10 μg·kg-¹·min-¹	+++	−	−	−	↑↑SVR
Vasopressin	0.02–0.04 U/min	Stimulates V1 receptors in vascular smooth muscle				↑↑SVR, ↔PVR
Inodilators
Dobutamine	2.5–20 μg·kg-¹·min-¹	+	++++	++	−	↑↑CO, ↓SVR, ↓PVR
Isoproterenol	2.0–20 μg/min	−	++++	+++	−	↑↑CO, ↓SVR, ↓PVR
Milrinone	0.125–0.75 μg·kg-¹·min-¹	PD-3 inhibitor				↑CO, ↓SVR, ↓PVR
Enoximone	2–10 μg·kg-¹·min-¹	PD-3 inhibitor				↑CO, ↓SVR, ↓PVR
Levosimendan	0.05–0.2 μg·kg-¹·min-¹	Myoflament Ca²+ sensitizer, PD-3 inhibitor				↑CO, ↓SVR, ↓PVR
CO indicates cardiac output; CS, cardiogenic shock; PD-3, phosphodiesterase-3; PVR, pulmonary vascular resistance; and SVR, systemic vascular resistance.

Initial Vasoactive Management Considerations in Types of Cardiogenic Shock (CS)

Cause or Presentation of CS	Vasoactive Management Considerations	Hemodynamic Rationale
Classic wet and cold	Norepinephrine or dopamine Inotropic agent	This subtype has low CI and high SVR. Consider hemodynamic stabilization with norepinephrine (preferred in ↑HR or arrhythmias) or dopamine (↓HR preferred but associated with higher risk of arrhythmias); Consider addition of inotropic agent when stabilized and after revascularization (MI only)
Euvolemic cold and dry	Norepinephrine or dopamine, Inotropic agent, Small fluid boluses	Consider hemodynamic stabilization with norepinephrine (preferred in ↑HR or arrhythmias) or dopamine (↓HR preferred but associated with higher risk of arrhythmias) Consider addition of inotropic agent when stabilized and after revascularization (MI only) LVEDP may be low, and patients may tolerate fluid boluses
Vasodilatory warm and wet or mixed cardiogenic and vasodilatory	Norepinephrine; Consider hemodynamics-guided therapy	This subtype has low SVR
RV shock	Fluid boluses, Norepinephrine, dopamine, or vasopressin, Inotropic agents, Inhaled pulmonary vasodilators	Hemodynamic goals include maintaining preload, lowering RV afterload (PVR), treating absolute or relative bradycardias, and maintaining atrioventricular synchrony Dopamine (↓HR preferred but associated with arrhythmia risk) Vasopressin may raise SVR and have neutral effect on PVR Consider adding or transitioning to inotrope after initial hemodynamic stabilization and revascularization
Normotensive shock	Inotropic agent or vasopressor	Initial inotropic therapy may be appropriate given that this subtype has SBP >90 mm Hg and relatively high SVR
Aortic stenosis	Phenylephrine or vasopressin; In patients with reduced LVEF, echocardiography- or PAC-guided dobutamine titration	Shock caused by aortic stenosis is an afterload-dependent state; Inotropy may not improve hemodynamics if LVEF is preserved; Definitive therapies will be defined by underlying cause and may include surgical aortic valve replacement or balloon valvuloplasty and/or transcatheter aortic valve replacement
Aortic regurgitation	Dopamine Temporary pacing	Maintaining an elevated HR may shorten diastolic filling time and reduce LVEDP; Definitive therapies will be defined by underlying cause and may include surgical aortic valve replacement
Mitral stenosis	Phenylephrine or vasopressin Esmolol or amiodarone	Shock resulting from mitral stenosis is a preload-dependent state; Avoiding chronotropic agents, slowing the HR (and thereby increasing diastolic filling time), and maintaining atrioventricular synchrony may improve preload; Definitive therapies will be defined by underlying cause and may include surgical mitral valve replacement or balloon valvuloplasty
Mitral regurgitation	Norepinephrine or dopamine Inotropic agents; Temporary MCS, including IABP	After hemodynamic stabilization with vasopressor, consider addition of inotropic agent; Afterload reduction may help reduce LVEDP IABP may reduce regurgitation fraction by reducing afterload and increasing CI Definitive therapies will be defined by underlying cause and may include surgical mitral valve replacement/repair and percutaneous edge-to-edge repair
Postinfarction ventricular septal defect	See classic wet and cold considerations Temporary MCS, including IABP	IABP may reduce shunt fraction by reducing afterload and increasing CI; Cardiac surgical referral for repair or percutaneous interventional umbrella closure
Dynamic LVOT obstruction	Fluid boluses; Phenylephrine or vasopressin; Avoid inotropic agents; Avoid vasodilating agents; Esmolol or amiodarone; RV pacing	Dynamic gradients may be reduced by increasing preload and afterload, reducing inotropy and ectopy, maintaining atrioventricular synchrony, and inducing ventricular dyssynchrony
Bradycardia	Chronotropic agents or Temporary pacing	Treatment should also focus on identifying and treating underlying cause of bradycardia; Chronotropic agents may include atropine, isoproterenol, dopamine, dobutamine, and epinephrine
Pericardial tamponade	Fluid bolus; Norepinephrine	Pericardiocentesis or surgical pericardial window required for definitive therapy
CI indicates cardiac index; CS, cardiogenic shock; HR, heart rate; IABP, intra-aortic balloon pump; LVEDP, left ventricular end-diastolic pressure; LVEF, left ventricular ejection fraction; LVOT, left ventricular outflow tract; MCS, mechanical circulatory support; MI, myocardial infarction; PAC, pulmonary artery catheter; PVR, pulmonary vascular resistance; RV, right ventricular; SBP, systolic blood pressure; and SVR, systemic vascular resistance.