Definition

Cardiac dysfunction leading to insufficient cardiac output and tissue hypoperfusion.

• Consider when SBP <90 mmHg sustained for >30 min (or vasopressors required) AND clinical or objective signs of tissue hypoperfusion (see below).
• Note: consider the diagnosis of normotensive cardiogenic shock when normal BP but rising lactate and transaminitis.

Identification of Cardiogenic Shock

Clinical: altered mental status, cold/clammy skin or extremities, decreased urine output

Objective: lactate >2.0mmol/L, UOP <30mL/hr, CI < 2.2 L/min*m², renal failure, transaminase elevation.

• Clinical pearl: elevations in biliary labs generally suggest venous congestion while transaminase elevations generally suggest underperfusion from shock. Creatinine elevations occur both from venous congestion and under perfusion so creatinine elevation is less useful as a biomarker for shock.

Cardiogenic Shock Phenotypes:

	Warm	Cold
Dry	Compensated Heart Failure	Primary Pump Dysfunction
Wet	Volume Overload (No shock)	Pump Dysfunction with Volume Overload

Wet: lower extremity edema, elevated JVP, pulmonary congestion (crackles, pulmonary edema on CXR), orthopnea.

Dry: no evidence of right sided volume overload has yet developed (normal JVP).

Clinical pearl: with transition from warm to cold, shift framework from neurohormonal blockade to hemodynamic stabilization (i.e. NO beta-blockers, ACE inhibitors when cold).

Etiologies of Cardiogenic Shock

• Myocardial infarction
• Acute decompensation of cardiomyopathy
• Severe valve disease (e.g. severe aortic stenosis, severe mitral stenosis, acute mitral insufficiency)
• Pericardial tamponade
• Arrhythmia
• Ventricular septal defect
• Myocarditis
• Pulmonary embolism
• RV failure
• Cardiotoxic medication
• Post-cardiotomy
• LVOT obstruction

Management

1) Stabilize

1. Initiate norepinephrine (over dopamine) as needed for perfusion.

• Although there is no specific MAP goal, >65 mmHg at first is reasonable.
• Vasopressor is a short-term fix; must initiate appropriate therapies, detailed below.

2. Obtain central venous access, arterial line, and consider PA catheter (clinically decompensating rapidly, mechanical circulatory support).

2) Calculate hemodynamics (Cardiac Index and Systemic Vascular Resistance)

• ABG for arterial oxygen saturation (SaO2).
• Mixed venous (from PA catheter, ideal) or central venous gas (from CVC) for venous oxygen saturation (SvO2).
• CBC (for Hb).
• Patient height and weight (to calculate BSA).
• Fick’s Formula:
  • BSA (body surface area) = [(Height (cm) x Weight (kg)) / 3600]^1/2
  • VO₂ (oxygen consumption) = 125 mL O₂/min x BSA
  • CO (Cardiac Output) (L/min) = VO₂/[(SaO2 – SvO₂) x Hb x 13.4] – Normal is 4-8 L/min.
  • CI (Cardiac Index) L/min/m² = CO/BSA – Normal is 2.5 -4.5 L/min/m².

• Thermodilution: requires a pulmonary artery catheter.
• SVR (Systemic Vascular Resistance) (dynes-sec/cm⁵) = 80 x (MAP – CVP)/CO
  • CVP should be obtained from CVC.

Note: for more detailed explanation of hemodynamics see Pulmonary Arterial Catheters section.

3) Initiate therapies: it is crucial to interpret the CI and SVR before starting therapy. The diagnosis of cardiogenic shock should be made with a low CI and high SVR.  

A. Inotrope initiation

• Goal: lactate clearance and ideally CI >2.
• Dobutamine: start at 2-3 mcg/kg/min.
  • Ensure norepinephrine is running/available to address potential vasodilatory response.
  • Wait at least ~60 minutes to assess effect given half-life of dobutamine.
  • DO NOT TITRATE INOTROPE TO MAP GOAL. TITRATE TO CARDIAC INDEX.
  • In general we recommend dobutamine over milrinone due to shorter half-life (easier initial titration) and renal dosing of milrinone (cardiogenic shock patients often have rapidly changing renal function).

B. Decongestion

• Evaluate volume status (i.e. wet or dry) by considering peripheral edema, pulmonary congestion, JVD elevation, IVC exam.
• Goal: CVP <10.
• Aggressive diuresis is indicated, would consider 3-4mg IV bumetanide (Bumex) +/- 250-500mg IV chlorothiazide (Diuril) (dosed 30 minutes prior). See Heart Failure section for further details on diuretics.

• Assess UOP at 2-3 hours.
• If insufficient UOP on max dose diuretics consider CRRT and nephrology consultation.

4) Reassess therapy/markers of perfusion: within 1-2 hours initially.

• CI, SVR, CVP, lactate
• Improving/stable: continue interventions, can space out hemodynamic monitoring labs (e.g. every 4 hours or every 6 hours).
• Worsening: increase inotrope (max dose dobutamine 5), add second inotrope (milrinone) consider mechanical circulatory support (see below) with rapid re-assessment of hemodynamics (e.g. 1-2 hours).
• Once lactate has cleared, hemodynamics are stable, and patient is effectively diuresing (if overloaded) can move forward to weaning inotrope.

5) Wean inotropes

NOTE: DO NOT turn off inotrope without weaning

Can begin weaning inotropes once the following conditions are met:

1. Stable dose of inotrope for approximately 24 hours.
2. Adequate decongestion.
3. Lactate cleared.

 

1. Start afterload reduction – hydralazine, nitroprusside, or ACE inhibitor (e.g. captopril)

• Hydralazine tends to be easiest to manipulate (e.g. start at 12.5mg PO q8h and uptitrate as tolerated with each dose).

• Soft blood pressures are expected but afterload reduction doesn’t necessarily cause hypotension - afterload reduction decreases SVR and concurrently increases cardiac output.
• Continue monitoring hemodynamics with each change (e.g. CV O2 saturation q12 hours).

2. Downtitrate inotrope – decrease dobutamine by no more than 1 mcg/kg/min over each 24 hour period (i.e. in increments of 0.5 mcg/kg/min every 12 hours) while increasing afterload reduction agent.
3. Initiation of neurohormonal blockade – do not start beta blockers and remainder of guideline directed therapies until at least 24 hours hemodynamically stable off inotropes with adequate afterload reduction therapy.

6) Refractory cardiogenic shock – LVAD and transplant

• With sustained cardiac failure, the only option for complete recovery is transplantation.
• LVAD’s are often considered “bridge to transplant” options, sustaining patients until an appropriate transplant might become available.
  • In certain cases they may also be used as a “destination therapy” to sustain patients who are not transplant candidates.
  • In some cases LVADs can be used as “bridge to decision” or “bridge to recovery” interventions.
  • LVAD implantation has clinical, anatomic, technical, and social requirements.
• Cardiac transplantation is a complex process with strict criteria for recipient listing, also frequently requiring committee evaluation for listing. Allocation is governed by severity of illness and time on the waitlist.

Etiology Specific Management

• ACS – emergent indication for revascularization.
• Aortic stenosis – valvuloplasty or valve replacement, PAC recommended, vasodilator.
• LVOT obstruction – preload dependence, avoid inotropy, increase preload/afterload.
• Cardiac tamponade – emergent pericardiocentesis.
• VSD – surgery vs percutaneous closure.
• Arrhythmia – anti-arrhythmic agents and cardioversion.
• Cardiotoxic medication – treat underlying ingestion (for details see Toxicology chapter).
• Myocarditis – primarily supportive, consider giant cell (biopsy and steroids can be beneficial).
• RV failure: therapies guided by invasive pressure monitoring, and consider small (250mL) fluid bolus to achieve higher CVP goal (i.e. 10-12).
  • Inferior MI, Pulmonary Embolism

Mechanical Circulatory Support

DISCLAIMER: please note that ALL operation and troubleshooting of mechanical circulatory support (MCS) should be made in conjunction with experienced operators (i.e. attending cardiologist).

At the time of drafting this handbook there are no randomized controlled trials supporting the use of mechanical circulatory support in cardiogenic shock. The IABP-SHOCK II registry in 2012 did not demonstrate a benefit to IABP placement over placebo in patients with acute MI complicated by cardiogenic shock. Retrospective and registry based data have suggested a utility to mechanical circulatory support devices in specific scenarios. Of note, Impella has shown promising results in myocardial infarction associated cardiogenic shock through the national cardiogenic shock initiative (NCSI) single-arm prospective registry. There is no randomized trial data supporting the use for mechanical circulatory support, only guideline opinions and expert consensus.

Left Ventricular Support

1. Intra-aortic balloon pump (IABP)
2. Impella (2.5, CP, 5.0)
3. TandemHeart
4. Venous-arterial extracorporeal membrane oxygenation (VA-ECMO)

Right Ventricular Support

1. Impella RP
2. VA-ECMO

   Device	Cardiac Output  (in L/m)	Mechanism	Insertion	Circulatory Support/Systemic Perfusion (MAP)	Ventricular Support (Unloading)	Coronary Perfusion (MAP – LVEDP)
   IABP	0.5	Winkessel Effect (Vacuum in aorta)	Percutaneous (arterial)	+/-	+/-	+/-
   Impella 2.5 Impella CP Impella 5.0	2.5 4.0 5.0	Axial Flow Pump via Archimedes screw (LV à Aorta)	Percutaneous (arterial) Percutaneous (arterial) Arterial cutdown	+ ++ +++	+ + +	+ + +
   Impella RP	4.0	Axial Flow Pump via Archimedes screw (RA à PA)	Percutaneous (vein)	++	++	-
   TandemHeart	3.5-5.0	Centrifugal Flow Pump (LA à systemic artery)	Arterial and venous, cutdown or percutaneous, with transseptal puncture	++	++	+
   VA-ECMO	6	Centrifugal Flow  (usually systemic artery and vein)	Arterial and venous, cutdown or percutaneous	++++	- (Loads LV)	+/-

   LV = left ventricle; LA = left atrium; CP = cardiac power; RP= right percutaneous
   Anticoagulation: in general is required for all MCS. IABP is the exception with institution-specific practices governing anticoagulation when placed at 1:1.

General indications:

• High-risk PCI
• Large acute MI
• Acute decompensated heart failure
• Cardiogenic shock
• Post-cardiac surgery
• Ventricular arrhythmias
• Massive PE
• Pulmonary hypertension

Indications for specific devices:

• IABP: preserved EF, multi-vessel CAD, aortic stenosis, mitral regurgitation.
• Impella: cardiogenic shock, ACS, high risk PCI with low LVEF, biventricular failure.
• TandemHeart: aortic regurgitation, profound hypoxemia, severe MR.
• VA-ECMO: profound hypoxemia, cardiac arrest, sepsis, multi-organ failure, biventricular failure.

Contraindications:

• IABP: aortic regurgitation (moderate or severe), severe PAD or aortic disease, aortic dissection.
• Impella: mechanical aortic valve, LV thrombus, severe PAD, inability to tolerate anticoagulation.
• TandemHeart: RA/LA thrombus, severe PAD, inability to tolerate anticoagulation.
• ECMO: inability to tolerate anticoagulation, severe PAD.

Complications:

In general, risk profile increases with complexity of insertion (particularly cannula size), overall device complexity, and level of anticoagulation.

• Limb ischemia
• Hemolysis
• Thromboembolism
• Bleeding
• Local vascular injury (cannula sites)
• Aortic injury (IABP)
• Cardiac tamponade (TandemHeart)
• RàL shunt (TandemHeart)
• Stroke

Weaning

• IABP: weaning is typically accomplished by reducing the ratio of augmented to non-augmented beats from 1:1 (max) to 1:2 to 1:3 with decreases every 3-6 hours. If doing well on 1:3 then return to 1:1, turn off anticoagulation and pull device.
• Impella: decreasing power (P) level, with P-8 being maximum corresponding to flow rate and rpms. At the P-2 level removal may occur.

Monitoring/Alarms

• IABP

1. Poor augmentation: may be due to loss of pulsatility (worsening LV failure), hypovolemia, or tachyarrhythmia (e.g. rapid atrial fibrillation).
2. Loss of balloon pressure: abnormal inflation waveform, blood in gas line (requires removal).

• Impella: positioning is monitored by echocardiography. A suction alarm may suggest positioning, ventricular thrombus, or decreased blood volume.
• TandemHeart and VA-ECMO are frequently managed by dedicated mechanical circulatory support services and monitoring/alarms are beyond the scope of this handbook.

Cardiogenic Shock Medications

Cardiogenic Shock Medications
Name (Receptor/Class)	Dose	Preload	PVR	PCWP	SVR	CO	Adverse Effects and Notes
Vasopressors
Phenylephrine a1	Start: 10 mcg/min 0 – 200 mcg/min	-	-	-	­­	-	Reserve only for patients with LVOT obstruction
Norepinephrine a1>b1>b2	Start: 2-5 mcg/min 0 – 30 mcg/min	-	­	-	­­	­	Dysrhythmia, Coronary vasospasm
Dopamine D  0.5-2 b1 5-10 a1 10-20	Start: 2 mcg/kg/min 0 – 20 mcg/kg/min	- - -	- - -	- - -	- ­ ­­	­ ­­ ­	Dysrhythmia
Epinephrine a1=b1>b2	Start: 2-5mcg/min 0 – 35 mcg/min	-	­/­­	-	­­	­­	Dysrhythmia, mitochondrial lactic acidosis
Vasopressin V1	Start: 0.01/0.04 0 – 0.04 units/min	-	­/¯	-	­­	-
Inotropic Agents
Dobutamine b1>b2>a1	Start: 2 mcg/kg/min 0 – 5 mcg/kg/min	-	¯	-	¯	­­	Tachyphylaxis Eosinophilic myocarditis
Milrinone PDE-3 inh	NOTE: RENAL DOSING Start: 0.125 mcg/kg/min 0 – 0.7 mcg/kg/min	-	¯	¯	¯	­	Dose adjustment in renal impairment Bolus can cause severe hypotension
Vasodilators
Nitroprusside Arteriolar dilator	Start: 0.1 mcg/kg/min 0.1 – 10 mcg/kg/min	¯	¯¯	¯¯	¯¯	­­	Generally safe for short periods Thiocyanate + MetHg toxicity Coronary steal in severe CAD
Nitroglycerin Venodilator	Start: 10 mcg/min 0 – 300 mcg/min	¯¯	¯	-	¯	-

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