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    Cardiogenic Shock

    Shahriar Lahouti
    October 5, 2023
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    67 min read

    5 October 2023 by Shahriar Lahouti.

    CONTENTS

    Introduction

    Cardiogenic shock (CS) is the most severe form of acute heart failure. It is a potentially complex, and hemodynamically diverse state of end-organ hypoperfusion that is frequently associated with multisystem organ failure. Despite improving survival in recent years, patient morbidity and mortality still remain high. This review will cover recent updates regarding the definition, underlying causes, pathophysiology, and management in light of recent literature with a focus on left ventricular failure.

    Epidemiology

    • The prevalence of cardiogenic shock (CS) varies according to the definition of CS, clinical setting care, and the era of data collection.
    • The prevalence of CS is ~15% in the intensive care unit (ICU)/ICCU *.
    • In-hospital mortality varies between 30% and 60% *. However, recent datasets reported lower mortality rates of ~37.5% *,*.
    • The epidemiology of CS has shifted from ACS-CS to decompensated HF (HF-CS) in the contemporary advanced CICUs.
      • While a decade ago, ACS accounted for ~80% of CS *, recent studies show that only 30% of CS cases are related to ACS *, and the remaining cases are associated with decompensated HF.
      • It is important to realize that there are differences between ACS-CS and HF-CS in terms of manifestation, management strategies, and prognosis.
        • The manifestation of HF-CS is different from those patients without preexisting HF who develop CS (e.g. some patients with AMI-CS) *.
          • Patients with chronic advanced HF may have compensatory adaptations that allow them to tolerate a degree of hemodynamic compromise that a patient without preexisting HF might not.
        • Non-ACS-CS patients have a greater burden of disease (more severe pre-existent HF, pulmonary hypertension, arrhythmias), but in-hospital survival is significantly better than ACS-related CS *, *.
        • In contrast, ACS has been shown to be a predictor of worse outcomes in patients with CS *.

    Definition

    Cardiogenic shock (CS) is a clinical diagnosis and refers to a complex clinical syndrome caused by an insufficient cardiac output resulting in a state of tissue hypoperfusion which, depending on its severity, may result in multi-organ dysfunction and death *. 

    • The clinical triad of CS includes *:
      1. Ineffective cardiac output (CO)
      2. Tissue and organ hypoperfusion
      3. Normal or elevated cardiac filling pressures (congestion)

    Shock is a state of hypoperfusion (defined by clinical and biochemical signs of hypoperfusion). Hypotension is not required for the definition of shock state *.

    • Patients in an early shock state can have normal-high BP (through a compensatory mechanism) while tissue perfusion may be significantly impaired *,*,*. Early recognition of hypoperfusion signs identifies ‘high-risk’ patients regardless of hypotension *.

    CS is a clinical diagnosis and hemodynamic parameters {e.g. reduced cardiac index (CI), elevated pulmonary capillary wedge pressure (PCWP)}, are not mandatory in clinical practice *,*.

    Basic cardiovascular physiology

    Cardiac output (CO) is the amount of blood pumped by the heart per minute and is affected by HR and stroke volume (SV).

    • CO = (SV x HR)/1000.
      • Cardiac output (L/min); stroke volume (mL/beat).
    • Cardiac output is dependent on heart rate and stroke volume.
    • Clinical hint💡
      • Bradycardia can directly pull down cardiac output and cause hemodynamic instability.
        • Severe bradycardia (e.g. HR< 30 bpm) should always raise concern for shock even in normotensive patients *.
      • Mild-moderate tachycardia will increase the cardiac output. 
        • ⚠️Do not suppress a sinus tachycardia. This is a compensatory mechanism in early circulatory derangement that may be keeping the patient alive.

    Stroke volume (SV) is defined as the volume of blood pumped out of the left ventricle during each systolic cardiac contraction. SV is affected by preload, myocardial contractility, and afterload.

    • Preload
      • Starling’s law of the heart or the Frank-Starling mechanism is shown in Figure 1A.
        • In a healthy physiologic state, increasing the length of myofibril (before contraction, i.e. preload) up to a certain limit will tend to increase cardiac contraction. This is referred to as preload responsive, i.e. increasing the preload results in increasing cardiac output.
      • Patients with congestive heart failure maintain their stroke volume close to normal at the expense of elevated left ventricular filling pressure (hypervolemia). Increased preload works here to keep stroke volume and cardiac index at a sub-optimal level (figure 1B).
        • Avoid overdiuresis in a patient with compensated heart failure who is doing fine clinically. This can cause a drop in stroke volume and cardiac index (figure 1B), contributing to the decompensation of CHF.
    • Contractility and afterload
      • Stroke volume and cardiac output depend on contractility and afterload as well. Increasing contractility or decreasing the afterload leads to increasing the stroke volume (figure 2).

    Arterial blood pressure is the inflow pressure for “organ perfusion”, therefore it provides an indirect measure of blood flow to the organs.

    • Mean arterial pressure (MAP) more closely reflects the entry pressure for perfusion of most vital organs *.
    • The relationship of MAP, CO, and systemic vascular resistance (SVR) is expressed mathematically as MAP = CO x SVR
    • Clinical hint 💡
      • Vasopressors raise MAP by increasing SVR. In a failing heart, this excessive afterload (↑SVR) is poorly tolerated, thereby “CO”  can progressively drop.

    Systemic vascular resistance (SVR) is the amount of force exerted on circulating blood by the vasculature of the body.

    • SVR ≈ LV afterload.
    • SVR can provide valuable information for distinguishing the classes of shock from each other. It is decreased in early distributive shock and is often increased in most other classes of shock (classes of shock,👉 here).
    • SVR= 80 x (MAP-RAP)/CO
      • Wherein SVR (dynes. sec/cm5 ); mean arterial pressure “MAP” (mm Hg), right atrial pressure “RAP” (mm Hg), and cardiac output “CO” (L/min).

    Pathophysiology

    Although etiologies of CS vary widely, the pathophysiology of CS comprises several unique but overlapping components to be considered.

    The following mechanisms may happen separately at different stages of CS, or each may occur simultaneously. The magnitude of the initial cardiac insult and/or early application of interventions may either mask or delay some of these stages.

    1. An initial cardiac insult that decreases cardiac output (CO)
      • Left and/or right ventricular dysfunction causes a drop in LV cardiac output and stroke volume, resulting in:
        • Hypotension
        • Elevated LV end-diastolic pressure *.
    2. Central congestion (elevated LV and/or RV filling pressures)
      • Vasoconstriction (including venoconstriction) will develop as a compensatory mechanism for hypotension. This will cause redistribution of blood volume into the circulating compartment, leading to elevated CVP and/or PCWP *.
      • Vasoconstriction causes elevation in afterload too.
      • Although vasoconstriction may superficially normalize the blood pressure, eventually the failing heart cannot handle the excessive preload and afterload. Therefore the LV output will drop further.
    3. Microcirculatory dysfunction
      • It is present early in CS, and may precede central hemodynamic congestion * (see appendix).
      • Mechanisms of microcirculatory dysfunction include: 
        1. Reduced cardiac output and increased vascular tone.
          • The microcirculatory network is “flow-dependent”. Reduced “CO” and vasospasm are potential contributing factors.
        2. Activation of systemic inflammatory response.
          • The cytokines and reactive oxygen species can cause diminished regional autoregulation leading to impaired microcirculation *.
      • Microcirculatory dysfunction results in reduced responsiveness to cellular metabolic demand, leading to tissue hypoxia *.
    4. Systemic inflammatory response syndrome (SIRS)
      • Clinically overt inflammation is seen in ~30% of CS patients by day 2 post-CS onset and may result in an initially reduced SVR *.
      • Mechanism of systemic inflammatory response activation:
        1. Primary cardiac insult can trigger a noninfectious inflammatory response.
          • For example, it has been well recognized that coronary plaque rupture can trigger the inflammatory cytokine release *,*.
        2. Concurrent infection: Approximately 25% of CS cases develop infection complications *. Risks for bloodstream infection include:
          • Vascular access
          • Hypoperfusion-related damage to the gut mucosal barrier and resulting bacterial translocation (BTL).
      • Activation of the inflammatory cascade is associated with further myocardial depression and interferes with catecholamine secretion *.
    5. Multi-organ dysfunction (MOD)
      • It can result from altered macrocirculation * and microcirculation *. MOD carries a poor prognosis.
      • Both “forward failure” (reduced cardiac output) and “backward failure” (venous congestion) contribute to the pathophysiology of organ failure (figure below).
    • The gut appears to be among the first organs involved in shock.
      • Microcirculatory injury in the intestinal barrier leads to increased bacterial translocation (BTL) *.
      • BTL results in the release of bacterial gram-negative lipopolysaccharides or endotoxins into the systemic circulation, which further perpetuates spirals of SIRS.

    💡More on Coronary Perfusion Pressure

    • Progressive reduction in coronary perfusion pressure (CPP) will happen due to the above mechanisms (#1-5). This causes a double-hit impact on myocardial performance, resulting in worsening myocardial function and progressive end-organ dysfunction.
    • Physiologic background
      • The left ventricle is perfused mainly in diastole.
        • Coronary perfusion pressure (CPP) of LV is defined as (DBP – LVEDP) *.
          • Systemic hypotension and elevated LVEDP have a cumulative impact on reducing LV perfusion.
      • The right ventricle is perfused in both systole and diastole.
        • CPP of RV in diastole is defined as (MAP– MPAP); where MAP, is mean arterial blood pressure; MPAP, is mean pulmonary artery pressure) *.
    • Clinical significance
      • These equations underscore the significance of raising CPP in hypotensive CS to prevent further myocardial damage. This should be done before the administration of inotropic medications.
      • Inotropic medications increase cardiac contractility, hence increasing O2 consumption and metabolic demands. Obviously, the blood flow should be optimized first (by raising CPP) before any attempts to optimize contractility.

    Etiology and precipitating factors of CS

    • Acute reduction in LV pump function
      • ACS
        • Large infarction (e.g. AMI with >40% loss of left ventricular mass) *.
        • Small/moderate infarction (e.g. AMI with <40% loss of left ventricular mass) with pre-existing dysfunction, extensive ischemia *.
        • Global ischemia
      • Tachymyopathy
      • Cardiomyopathies *
        • Ischemic and hypertrophic cardiomyopathy, Takotsubo cardiomyopathy.
      • Myocarditis (e.g. viral and bacterial infections, reactions to medications, and underlying autoimmune diseases).
      • Stunned myocardium from prolonged ischemia (e.g. cardiac arrest, hypotension, cardiopulmonary bypass).
      • Pregnancy-associated heart disease *
        • Peri-partum cardiomyopathy
        • Coronary artery dissection
    • Arrhythmia
      • Tachyarrhythmia (most often new-onset atrial fibrillation) *.
      • Bradyarrhythmia.
    • RV dysfunction. These can happen alone or in association with left-sided pathologies (preexisting LV dysfunction, or concurrent LV dysfunction) *
      • RV dysfunction secondary to RV pump failure: RV infarction, progressive cardiomyopathy, septic cardiomyopathy *.
      • RV dysfunction secondary to pulmonary vascular disease: Worsening pulmonary hypertension, acute pulmonary embolism.
    • Valvular or mechanical dysfunction
      • Native valve dysfunction (e.g. endocarditis, ruptured papillary muscle)
      • Prosthetic valve dysfunction (e.g. thrombosis)
      • LV outflow tract obstruction (LVOTO)
      • Ventricular septal defect or free wall rupture.
      • Intracardiac mass (e.g. left atrial myxoma causing obstruction to LV filling) *, thrombi, tumor metastasis.
    • Pericardial disease *
      • Tamponade
      • Progressive pericardial constriction
    • Volume alteration
      • Volume overload (diuretic non-adherence, dietary indiscretion) *.
      • Acute hypovolemia (e.g. over-diuresis, reduced oral intake, gastroenteritis) *.
    • Non-adherence with HF medications *
    • Iatrogenic
      • Cardio-depressant sedatives (e.g. propofol)
      • Excessive use of diuretics
      • Excessive volume loading in RV shock
    • Other
      • Uncontrolled hypertension
      • Thyroid disease (both hyperthyroidism and hypothyroidism)
      • Toxidromes e.g. β-blockers, calcium channel blockers, digoxin, antiarrhythmics toxicity *.
      • Checkpoint inhibitors

    Approach to diagnosis of CS

    The initial diagnostic approach and medical stabilization are usually started in the ED. The framework for the diagnosis of CS involves:

    1. Is this patient in a hypoperfusion state (shock state)?
    2. Does this patient with hypoperfusion have cardiogenic shock?
    3. How severe is this cardiogenic shock?
    4. Is this patient with low cardiac output in cardiogenic shock?
    Is this patient in a hypoperfusion state (shock)?

    Evaluate for evidence of hypoperfusion

    The clinical and biochemical evidence of hypoperfusion is mentioned here. However, these are not universally present through different stages of CS and also are not highly specific for hemodynamic derangement *.

    Skin perfusion status: Cool/clammy/mottled extremities and sluggish CRT are suggestive of low CO.

    • Cool, clammy skin is due to compensatory peripheral vasoconstriction that redirects blood centrally, to maintain vital organ perfusion *.
      • Caveats:
        • A cool, clammy, or cyanotic skin may also be due to the underlying peripheral arterial disease.
        • A warm, hyperemic skin does not exclude the absence of shock because such an appearance may be present in early distributive shock (pathologic vasodilation, vasoplegia).
    • Mottling is less sensitive, but more specific for hypoperfusion and increased mortality *,*,*.
      • A cyanotic, mottled appearance is a late and worrisome feature of shock.

    Brain: Altered level of consciousness (LOC) and mentation.

    • Altered LOC and delirium are not specific symptoms of cerebral hypoperfusion *.
      • This can happen due to intracranial pathologies or more commonly secondary to toxic and metabolic disturbances.
    • Normal mentation doesn’t prove that perfusion is adequate.
      • For example, some patients in occult CS may have normal mentation despite profoundly low cardiac output.

    Kidney: Doubling creatinine over baseline and urine output <30 mL/h.

    • Approximately 25% of patients with CS develop AKI *.
    • AKI has diverse causes with several non-hemodynamic contributors such as infection, iatrogenic damage (e.g. contrast media, nephrotoxic medication), and elevated intra-abdominal pressure *.

    Liver: Transaminitis

    • Only 25% of patients with CS have an abnormal liver function test in the acute phase *.
    • Derangement in liver function tests is not specific for hypoperfusion and the differential diagnosis is diverse.
    • In the setting of CS, abnormal liver function test results would be observed under both reduced perfusion (ischemic hepatitis, aka shock liver) and venous congestion (congestive hepatopathy):
      • Congestive hepatopathy (due to elevated RAP)
        • Mild-moderate transaminitis with elevated ALP x2-3 UNL.
        • Elevated direct and indirect bilirubin with total bilirubin level often < 3 mg/dL *.
      • Shock liver (ischemic hepatitis)
        • Severely elevated AST (> x10 UNL) *.
        • Severe hyperbilirubinemia with a total bilirubin level as high as 15-20 mg/dL *.
        • Markedly ↑LDH. Increased LDH tends to be massive and an ALT/LDH ratio of <1.5 helps distinguish ischemic injury from other forms of acute hepatitis *.
        • Mild-moderate ↑ALP is also reported. 

    Blood pressure: SBP <90 or MAP <60 or >30 mmHg drop from baseline.

    • Shock is a state of hypoperfusion. However, hypoperfusion is not synonymous with hypotension.
      • For example, in patients with normotensive CS, SBP is >90 mm Hg despite the presence of clinical and biochemical evidence of hypoperfusion.

    Tachycardia (a PR >100 bpm) *.

    • Generally, both pulmonary edema and systemic hypoperfusion are hyperadrenergic states.
    • Tachycardia is a compensatory response to underlying hemodynamic derangement. However, components of compensatory response may be blunted in patients who are using cardio-depressant medications, e.g. β-blockers.

    Bradycardia

    • Marked bradycardia (e.g. HR<40) should always raise concern for shock even in normotensive patients.
    • Relative bradycardia.
      • In cardiogenic shock, a HR in the range of 90-110 bpm is expected. HR < 80 is called relative bradycardia in patients with CS and may provide diagnostic clues for the underlying cause(s), such as:
        • Hyperkalemia
        • Inferior AMI
        • Intoxications: β-blockers, calcium channel blockers, digoxin *.
        • Conduction abnormalities

    Shock Index >>0.8 can suggest hemodynamic instability.

    • Shock index may be insensitive in the presence of negative chronotropic medications (e.g. beta-blockers), conduction system disease, and inferior AMI.

    Arterial lactate ≥ 2mmol/L

    • Lactate elevation is not very sensitive for diagnosis of shock.
      • For example, lactate can be normal in shocked patients who have inadequate sympathetic nervous function.
    • Elevated lactate is very nonspecific and has many false positives such as liver failure, seizures, and β-2 receptor stimulation (e.g. epinephrine, albuterol administration) *,*. More on this, here.

    Diagnostic pitfalls

    • There is no sign, symptom, or lab test that is entirely sensitive or specific for shock (explained above).
    • Diverse clinical presentation
      • The clinical presentation of shock is not uniform. Shock is a physiologic continuum that can progress through several stages with different clinical presentations. These clinical stages include pre-shock (occult shock), overt (established) shock, and refractory shock * (figure below).
    stages of shock
    • Shock is often multifactorial
      • Many patients with shock have a combination of more than one form of shock. For example, a patient with cardiogenic shock who develops septic complications.
    • Overlapping pictures
      • Certain forms of shock share overlapping features (e.g. late septic shock may look quite similar to advanced cardiogenic shock).
    Does this patient with hypoperfusion have cardiogenic shock?

    As explored above signs and symptoms of hypoperfusion might not help to identify the cardiogenic cause of shock. In the next few sentences, the distinguishing features of cardiogenic shock are discussed.

    Diagnostic clues for cardiogenic cause of shock

    1.Low cardiac Index

    • The core feature of CS is ineffective cardiac output. 
    • Pay attention to pulse pressure. A narrow PP (PP< SBP/4) may indicate a low CO *.
    • Perform echocardiography
      1. The presence of a hyperdynamic heart 📖 will rule out CS.
      2. Cardiac output can be measured by echocardiography.
        • A low CI (e.g. < 2.2 L/min/m2) is the key finding in CS with different hemodynamic phenotypes.

          • Caveat: Although CI thresholds <1.8 to 2.2 L/min/m2 have been proposed for CS, absolute cutoffs are likely impractical given that end-organ hypoperfusion with higher CIs has been documented *.

    2.Elevated left atrial pressure (pulmonary congestion)

    • Elevated left atrial pressure reflects the wet (pulmonary edema) feature of cardiogenic shock.
    • Clinical clues for elevated LAP: Dyspnea, orthopnea, and rales in lung fields.
    • Biochemical markers: ⬆️BNP.
      • A low BNP level argues against CS in the setting of hypotension; however, an elevated BNP level is not helpful in establishing the diagnosis of CS *.
    • Echocardiography: Assessment of mitral inflow velocities
      • In patients without systolic dysfunction, a septal E/e’ >15 is highly suggestive of elevated LAP; while an E/e'<8 reflects normal LAP *.
        • E/e’ between 8-15. This range can be used as a spectrum. A value closer to 8 suggests a lower LAP, and a value closer to 15 is suggestive of a higher LAP.
      • In patients with systolic dysfunction (↓LVEF), use E/A ratio. An E/A > 2 is suggestive of elevated LAP.
    • Lung ultrasound (LUS): Diffuse bilateral B-lines on LUS may suggest ↑LAP.

    3.Hypervolemia (systemic congestion)

    • Patients with chronic heart failure often have systemic congestion. Elevated right-sided filling pressure may reflect volume overload.
      • Note that CS has different hemodynamic phenotypes. They share a common feature which is reduced cardiac index *.
      • Elevated right-sided filling pressure could be present in certain phenotypes. Having said that, a normal central venous pressure does not exclude CS *.
    • Clinical clues: Jugular venous distension (JVD), peripheral edema, ascites, pleural effusion, and pericardial effusion.
    • Biochemical markers: ⬆️BNP, abnormal renal and liver function test (congestive hepatopathy, nephropathy).
    • Enlarged IVC size with decreased respiratory collapsibility.
    • A higher grade on the VExUS score. More on this👉 here.

    Diagnostic approach to CS

    Collect and collaborate data (multidimensional evaluation)

    • Obtain history, physicals (e.g. vitals, signs and symptoms of hypoperfusion and congestion), labs, and bedside ultrasound/echo information.
      •  Labs:
        • CBC, electrolytes, LFTs, lactate, TSH (if thyroid disease is suspected), and digoxin levels (for patients on digoxin).
        • Troponin, BNP. 
        • 12-lead ECG.
      • Imaging: Echocardiography, IVC, ultrasound of the lung/abdomen.
        • Echocardiography should be used to determine the underlying diagnosis, guide interventions, and monitor response to therapies (figure below).
          • The first-line echo should be performed in ED as per FoCUS protocols (FoCUS protocols and challenges )
          • More comprehensive echocardiography should be performed as early as possible. More on this,👉 here.
    echocardiography in cardiogenic shock

    Summary of in-hospital monitoring and investigations *

    Differential diagnosis

    DDx of shock

    • Determine the physiologic class of shock, based on integrated findings (table below).
      • Keep in mind that patients with multiple chronic problems or multifactorial shock may defy classification.
    • Exclude the following conditions which require a different set of treatments. 
      • Obstructive shock (e.g. pulmonary embolism, tamponade).
      • Structural abnormalities: Valvular emergencies, dynamic left ventricular outflow tract obstruction (LVOTO), intracardiac mass?
      • Aortic dissection. Is the aortic root enlarged? Look for signs of aortic direction including direct signs (intimal flap) and indirect signs (e.g. aortic regurgitation, pericardial effusion, and pleural effusion). More on this, here.
    physiologic classification of shock at bedside

    DDx of pulmonary edema

    • The etiologies of pulmonary edema (based on its pathophysiology) are represented below. The two predominant pathophysiologic mechanisms that can cause pulmonary edema include:
      • ↑Hydrostatic pressure (e.g. cardiogenic pulmonary edema), and
      • ↑Permeability pulmonary edema (e.g. ARDS) *,*.
    • Perform echo and lung ultrasound to distinguish these two subtypes of pulmonary edema.
    • Echo: Generally, the most helpful variable that can differentiate these two subtypes of pulmonary edema is the left atrial pressure (LAP).
      • Elevated LAP is the core feature of hydrostatic pulmonary edema. A septal E/e’ >15 is highly suggestive of hydrostatic pulmonary edema. More on this,👉 here.
    • Lung ultrasound: The presence of B-lines might suggest pulmonary edema *. Helpful clues to differentiate hydrostatic vs. permeability pulmonary edema on lung ultrasound are discussed here.
      • Hydrostatic pulmonary edema
        • The B-lines are bilateral and symmetric.
          • Asymmetric B-lines sometimes are present in cardiogenic pulmonary edema (2.1%) *.
            • This will cause an A/B profile on lung ultrasound (slides below).
            • It can be seen in severe “mitral regurgitation” *.
            • Usually, it is right-sided pulmonary edema, but rarely left-sided pulmonary edema can happen (figure below).
            • Unilateral pulmonary edema is related to an independently increased risk of mortality and should be promptly recognized to avoid delays in treatment *.
        • Presence of lung sliding.
        • Thin and regular pleural lines.
        • Pleural effusion(s), usually bilateral.
          • Generally, pleural effusion denotes chronicity of heart failure syndrome.
          • Effusion is transudative. The absence of plankton sign/hematocrit sign is typical for transudative effusions.
    cardiogenic shock
      • Increased permeability pulmonary edema
        • The B-lines could be bilateral or unilateral.
        • Lung sliding is present but may be diminished due to inflammation.
        • Pleural lines are thick and irregular with or without subpleural consolidation.
        • Pleural effusion(s), if present, is exudative.
          • Mechanism: Increased vascular permeability from inflammation/infection/malignancy
          • Lung ultrasound appearance: The presence of plankton sign/hematocrit sign is suggestive of exudative effusion.
    How severe is this cardiogenic shock?

    Five evolutionary stages of CS have been described by the Society for Cardiovascular Angiography and Interventions (SCAI) *.

    • This classification can be applied rapidly bedside upon patient presentation, across all clinical settings.
    • The SCAI classification establishes a unifying system for grading the severity of CS.
    • It uses bedside clinical assessment of hypoperfusion, measurement of lactate level, and hemodynamic evaluation.
    • Patients with acute cardiovascular disease are stratified into 5 SCAI shock stages of escalating severity*.

    A: At risk

    • A hemodynamically stable patient who is not currently experiencing signs or symptoms of CS, but is at risk for its development (e.g. large AMI, decompensated heart failure).
    • Exam: Normal mentation, warm and well-perfused extremities with strong distal pulses, clear lung sound, and normal JVP.
    • Labs: Normal lactate, normal (or at baseline) renal function.
    • Hemodynamic: Normotensive (SBP ≥100 mmHg or at baseline).
      • If invasive hemodynamics are assessed:
        • CI ≥2.5 L/min/m2 (if acute).
        • CVP ≤10 mmHg.
        • PCWP ≤15 mmHg.
        • PA saturation ≥65%

    B: Beginning (pre-shock=occult shock)

    • Unstable hemodynamic (such as hypotension or compensatory tachycardia) WITHOUT hypoperfusion (Hypotensive Normoperfusion).
      • Patients with preserved perfusion despite significantly abnormal invasive hemodynamics (such as reduced CI) are also classified as SCAI stage B.
    • Exam: Normal mentation, warm and well-perfused extremities with strong distal pulses, rales in lung fields, JVD (mild volume overload).
    • Labs: Normal lactate, minimal acute renal function impairment, ⬆️ BNP.
    • Hemodynamic: Hypotension (SBP<90, or MAP<60, or > 30mm Hg drop from baseline), OR Tachycardia (pulse ≥100) *.
      • If hemodynamics are done:
        • CI ≥2.2 L/min/m2 (if acute)
        • PA saturation ≥65%

    C: Clasic CS

    • A patient who manifests with hypoperfusion and who requires an initial set of interventions (inotropes, pressor, mechanical support including ECMO) beyond volume resuscitation. These patients typically present with relative hypotension (but hypotension is not required, therefore normotensive CS will be classified as stage C).
    • Exam: Looks unwell, delirious, acute alteration in mental status, cold and clammy extremities, sweating, mottling may be present, volume overload, extensive rales.
    • Labs: Lactate ≥2 mmol/L, ⬆️Creatinine to 1.5 x baseline (or 0.3mg/dL) or > 50% drop in GFR, ⬆️LFTs, ⬆️BNP.
      • Lactate is commonly used to detect hypoperfusion but may be dissociated from hemodynamics in cases such as chronic HF where patients may have a normal lactate level with a depressed cardiac index.
      • Generally, arterial lactate >2 mmol/L is consistent with at least SCAI SHOCK stage C, although some patients may demonstrate other manifestations of end-organ hypoperfusion with a normal lactate level, and there are also causes of an elevated lactate level other than shock, such as mesenteric ischemia or compartment syndrome
    • Hemodynamic: May include any of the following:
      • SBP <90 (or MAP <60, or >30mm Hg drop from baseline), OR Tachycardia; AND drugs/devices used to maintain BP above these targets.
      • If invasive hemodynamics are assessed (strongly recommended) *:
        • CI < 2.2 L/min/m2
        • PCWP >15 mmHg
        • RAP/PCWP ≥ 0.8 *
        • PAPI <1.85 *
        • Cardiac power output ≤0.6 *
      • Note that patients with established CS can be further subcategorized as LV-dominant, RV-dominant, or biventricular shock. These will produce different hemodynamic profiles (shock profile). This is discussed more in Forrester classification for hemodynamic phenotyping. A summary of the hemodynamic phenotype (shock profile) is provided below.
    • The distinction between SCAI SHOCK stages B and C is critical.
      • Patients with hypoperfusion in the absence of hypotension (normotensive CS; classified as stage C in SCAI) are at higher risk of dying than patients with hypotension and preserved perfusion (hypotensive normoperfusion; classified as stage B in SCAI) *.
        • The stage B (pre-shock: Hypotensive Normoperfusion“) may occur in severe AHF.
          • Hemodynamic: SBP < 90 mm Hg, CI ≥2.2, SVR 800–1600 dynes-s/cm –5.
          • Absence of overt clinical signs and symptoms of hypoperfusion.
          • Lactate levels and labs are normal.

    D: Deteriorating

    • A patient who has failed to stabilize despite intense initial efforts.
    • Classification in this stage requires that a patient meet the following conditions *:
      • The patient has had some degree of appropriate treatment/medical stabilization.
      • At least 30 min have elapsed, but the patient has not responded with hypotension or end-organ hypoperfusion resolution.
      • The patient requires further escalation (escalation is an increase in the number or intensity of IV therapies to address hypoperfusion or the addition of MCS) to maintain perfusion.
    • Exam: Any of stage C and worsening (or not improving) signs/ symptoms of hypoperfusion despite the initial therapy.
    • Labs: Any of stage C and lactate rising and persistently >2 mmol/L, deteriorating renal function, worsening LFTs, rising BNP.
    • Hemodynamic: Any of stage C AND requiring escalating doses OR increasing numbers of pressors or the addition of a mechanical circulatory support device to maintain perfusion.

    E: Extremis

    • A patient who meets any of the following conditions:
      • If perfusion cannot be restored using multiple simultaneous vasoactive drugs and/or MCS devices (refractory Shock), or
      • Patients with refractory shock impending circulatory collapse, or
      • Cardiac arrest with ongoing cardiopulmonary resuscitation (CPR), or
      • Refractory cardiac arrest with ongoing CPR.
    • Exam: Typically unconscious, near pulselessness, cardiac collapse, defibrillator used, mechanical ventilation.
      • Stage E prospectively is a patient with cardiovascular collapse or ongoing CPR *.
    • Labs: Lactate ≥8 mmol/L, CPR (A-modifier), severe acidosis (e.g. pH <7.2) , base deficit > 10 mEq/L *.
    • Hemodynamic: Hypotension despite maximal support, no SBP without resuscitation, PEA or refractory VT/VF, need for bolus doses of vasopressors.
    • The SCAI classification is validated in a large cohort of unselected intensive cardiac care unit (ICCU) patients providing robust mortality risk stratification regardless of CS etiology, in a manner that was amplified by the presence of CA *.
    • Additional prognostic variables (besides classification staging) *
      1. Age
      2. The trajectory of SCAI. This classification is inherently dynamic, and a rising or persistently elevated SCAI Shock stage portends worse outcomes *.
      3. Duration of time spent in higher SCAI Shock stages *,*.
      4. Cardiac arrest
        • However, cardiac arrest events are heterogeneous, and single defibrillation for a brief ventricular arrhythmia without CPR and normal neurologic function does not change the prognosis of a patient with CS *. Instead, two aspects of cardiac arrest can change the prognosis:
          1. Neurologic status (awake or comatose) and
          2. Physiologic impact of the arrest, as prolonged CA may fundamentally change the patient trajectory if ischemia-reperfusion heralds multiorgan
            failure.
        • It has been suggested that cardiac arrest can portend worsening of prognosis only if the patients sustained an anoxic brain injury, evidenced by a GCS <9; alternatively, the absence of a motor response to voice (i.e. not following commands) is a helpful definition *.
    Phenotyping the CS
    • Background
      • Most patients with advanced HFrEF have a low cardiac index (CI< 2.2 L/min/m2); however, they do not have CS.
        • Patients with chronic compensated heart failure may be doing well clinically with elevated systemic vascular resistance.
        • In contrast, patients with a higher CI (CI>2.2 L/min/m2) can have signs and symptoms of hypoperfusion *.
      • Moreover, there are different hemodynamic phenotypes for CS * determined by:
        1. Type of cardiac involvement (left vs. right) *.
          • CS can be further characterized as LV-dominant, RV-dominant, or biventricular shock, each of which may present differently and warrant different treatment strategies *.
        2. Presence of the systemic inflammatory response syndrome *,*.
    • Use Forrester classification for hemodynamic phenotyping of CS (figure below).
      • These formal definitions of hemodynamic shock phenotypes may help guide therapy and improve outcomes *.
      • Hemodynamic phenotyping (shock profile) can be performed based on the cardiac index and pulmonary capillary wedge pressure. Patients may be categorized as shown in the following figure.
        • Assess for clinical signs and symptoms of hypoperfusion, and congestion.
        • Perform echocardiography and lung ultrasound to evaluate the left and right ventricular function, and evidence of congestion (invasive hemodynamic evaluation might be required for a certain group of patients).
        • Note that CS has a complex and dynamic pathophysiology. The patient may go from one category to another.
      • The common physiological characteristic is a low cardiac index (CI), but pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), and systemic vascular resistance (SVR) may vary *.
    • There are two other uncommon but hemodynamically distinct entities overlaid on this framework: Normotensive CS and right ventricular CS (which will be covered in the following discussion).
    Classic CS
    • Most common reported CS phenotype in AMI-CS (~70%) *.
    • Hemodynamic profile: ↓CI {systemic hypoperfusion (cold)}, ↑PCWP (wet lung)}.
    • Cardiogenic shock patients may look misleadingly fine, but they are indeed critically ill.
    • Patients in classic CS cannot be managed with volume administration or removal (figure below).
      • Giving volume will worsen their pulmonary congestion (making them more wet).
      • Removing volume will worsen their systemic hypoperfusion (making them more cold).
    • Therefore, management of these patients usually requires interventions to improve cardiac function (e.g. inotropes, revascularization, or mechanical support).
    • Early diagnosis facilitates appropriate critical management.
      • Patients with unrecognized CS will generally fail to respond to non-intensive therapy. Undiagnosed patients often run in vicious circles (the patient is initially managed with fluid removal, then develops worsening renal failure, then is given fluid back, and then develops pulmonary edema).
    Vasodilatory CS or Mixed Shock
    • 20% of patients in the SHOCK trial had low SVR at the onset of CS *.
      • In patients with AMI-CS, mixed CS appeared to be associated with higher mortality and morbidity *.
    • Hemodynamic profile: Concomitant ↓SVR and ↓CI *.
    • Pathophysiologic processes that can lead to vasodilatory CS *
      • A noninfectious inflammatory response.
        • For example, the coronary plaque rupture can trigger the inflammatory cytokine release *,*.
      • Concurrent infection.
      • Metabolic derangements such as multiorgan failure and acidosis (sometimes termed hemometabolic CS).
      • Vasoplegia * after cardiac arrest (CA) or cardiac surgery.
      • Vasodilatory medications.
      • Interpatient differences in the immune response to acute insults.
    • As explained above, activation of systemic inflammatory response commonly occurs in CS.
      • In essence, the final common pathway of all types of shock is micro-circulatory alteration mediated by activation of systemic inflammatory cascade *.
      • This also accounts for the fact that different classes of shock can not be differentiated in later stages *.
      • Keep in mind that some patients with septic shock may develop a septic cardiomyopathy. Read more on this 📖.
    • Patients who are warm/wet may often be managed with diuresis and/or vasodilation to reduce their afterload (vasodilation shifts fluid out of the lungs without affecting the total body volume).
    Euvolemic (or hypovolemic) CS
    • It is most commonly seen in diuretic-responsive patients with chronic HF and subacute decompensation. However, it also represents 28% of patients with AMI-CS *,*.
    • Hemodynamic profile: ↓CI (hypoperfused=cold) and ↑SVR.
    • Patients with compensated CHF maintain their stroke volume at the expense of a higher preload (hypervolemia). Overdiuresis can lead to decompensation by pulling down the stroke volume and “CO” (figure 1B).
    • Compared with patients with classic CS, those with euvolemic CS were less likely to have had a previous MI or CKD and had significantly lower PCWP *.
    • Patients who are cold/dry may often respond to fluid administration by increasing stroke volume (figure above) *.
    Normotensive CS
    • 5.2% of CS in the SHOCK trial registry *.
    • Hemodynamic profile
      • They have a “comparable” CI, PWCP but a higher SVR compared with hypotensive patients with CS (accounting for relatively higher blood pressure).
      • Typically, ↓CI (hypoperfused), ↑/⬌PCWP.
      • SBP is kept >90 mm Hg at the expense of an elevated SVR.
      • Lactate ≥ 2mmol/L
    • Clinical significance: There is a risk of potential hypoperfusion without profound hypotension *. See media below.
    • SCAI classification of CS nicely classifies these patients at stage C and distinguishes them from “Hypotensive Normoperfusion” patients (SCAI stage B).
    Biventricular or RV-predominant CS
    • 5.3% of patients with MI-induced CS *.
    • Biventricular dysfunction (either as RV-predominant or LV-predominant CS) is associated with worse outcomes compared with CS due to “isolated” LV failure *,*.
    • Hemodynamic profile: They may present as ‘wet-cold’ or ‘wet-warm’*. 
      • Relatively higher C, and LVEF, with NO differences in CI or PCWP.
      • Different values of SVR according to the extent of systemic inflammatory response.
      • Pulmonary artery pressure *:
        • If the cause of biventricular CS is predominantly RV pump failure (e.g. RV myocardial infarction): Pulmonary artery pressure is usually low or normal.
        • If the cause of biventricular failure is predominantly elevated RV afterload (e.g. pulmonary embolism, Type 1 PH): Pulmonary artery pressure is elevated.
        • If the cause of biventricular CS is predominantly LV failure (e.g. Type 2 pulmonary hypertension= PVH): Pulmonary artery pressure is elevated.
    • The severity of the RV instability can be assessed by calculating the pulmonary artery pulsatility index (PAPI).
      • PAPI= (PASP-PADP)/RAP. 
        • Where PASP, is pulmonary artery systolic pressure; PADP is pulmonary artery diastolic pressure; RAP, is right atrial pressure.
      • A PAPI ≤1 identifies patients with severe RV dysfunction *.

    Hemodynamic evaluation

    Principles

    • No single hemodynamic variable is sensitive and/or specific enough to be used for identifying cardiovascular insufficiency *. Multidimensional assessment can circumvent this pitfall.
    • All hemodynamic variables should be interpreted in a “clinical context”.
      • For example, a patient with chronic compensated heart failure may be doing well clinically with an elevated systemic vascular resistance (SVR). The elevated systemic vascular resistance works here as a compensatory mechanism, allowing the maintenance of adequate blood pressure.
    • The current concept of functional hemodynamic monitoring encourages dynamic assessment of hemodynamic variables in response to treatment *.
    • For a complete discussion, refer👉here.

    Non-invasive hemodynamic assessment

    • It is essential for the initial diagnosis and management of patients with CS *.
    • Note that a complete hemodynamic assessment and the adequacy of end-organ and tissue perfusion in response to individualized targets can be made by integrating serial markers of systemic perfusion,* echocardiography, and ultrasound of the abdomen and lung *. More on this, 👉here.

    Pulmonary artery catheterization (PAC)

    • Routine use of PA catheterization is not recommended by AHA guidelines, even in CS *.
      • PAC is an invasive procedure with the associated risk of complications (table 1👉 📖).
      • With the advent of non-invasive monitoring, i.e. echocardiography, medical staff are less skilled at insertion and troubleshooting of PA catheters. For technical aspects of accurate PAC hemodynamics (table 2 👉📖).
      • PAC always reveals abnormal numbers, but it’s unknown what should be done with this data (read this fantastic article; “Alice in intensiveland”) *.
        • For example, there is no defined goal for cardiac output or systemic vascular resistance. A cardiac index that may be adequate for one patient will leave another patient in cardiogenic shock.
    • Possible indications for PAC
      • Unresponsiveness to initial therapy.
      • Documentation of hemodynamics to determine candidacy for cardiac transplantation or ventricular assist device.
      • Uncertain nature of shock (mixed shock) with no alternative source of hemodynamic information (e.g. poor TTE windows and inability to perform a TEE) *.
    • Contraindications to PAC
      • Bundle branch block (especially left bundle branch block), since PA catheterization may cause right bundle branch block *.
      • Arrhythmia or hyperkalemia (insertion may trigger arrhythmias).
      • Risk of displacing other devices (e.g. transvenous pacemaker).
      • Prosthetic or stenotic tricuspid/pulmonic valve.

    Normal value of hemodynamic variables (pulmonary artery catheter data): See appendix *.

    • Directly measured parameters by PAC include CVP; pulmonary artery systolic pressure (PASP); pulmonary artery diastolic pressure (PADP); PCWP, which is also commonly referred to as pulmonary arterial occlusion pressure; cardiac output by thermodilution and mixed venous oxygen saturation (SvO2).
    • Derived parameters: In addition to directly measured parameters, derived parameters (e.g. systemic vascular resistance and pulmonary vascular resistance) can be calculated. Some of these derived parameters that have prognostic significance and can be used to tailor therapy for patients with CS are discussed here *.
    • Markers of cardiogenic shock
      • Cardiac Power Index (CPI)
        • CPI is an indicator of significant ventricular dysfunction and has proven to be a strong hemodynamic predictor of poor outcome at CPI < 0.4 W/m2 *.
        • Cardiac Power Index (CPI) = MAP x CI/451 (Watts/m2).  Normal: 0.5-0.7 Watts/m2
    • Markers of RV function
      • Pulmonary artery pulsatility index (PAPI)
        • Pulmonary artery Pulsatility Index (PAPI)= (PASP-PADP)/RAP.
        • A PAPI ≤1 (in AMI) or <1.85 (after LVAD *) identifies patients with severe RV dysfunction *.
      • RAP/PCWP ratio
        • Under normal conditions, central venous pressure (CVP) is significantly less than pulmonary capillary wedge pressure (PCWP).
        • A RAP/PCWP >0.86 (in AMI), or >0.63 (after LVAD *) is suggestive of impaired RV function, though this index is more specific if CVP itself is elevated above normal .*

    The hemodynamic profiles of cardiogenic shock subtypes are summarized below.

    Management

    Chain of survival

    The chain of survival of cardiogenic shock is shown below. For optimal outcomes, all links in the chain are optimally required including:

    • Early diagnosis.
    • Early cardiovascular and hemodynamic support (medical treatment and mechanical circulatory support, to buy time for definitive treatment).
    • Early intervention (e.g. early revascularization for AMI-CS) to reverse the cause.
    cardiogenic shock chain of survival

    System of care

    • A model analogous to primary PCI pathways has been proposed by the American Heart Association to facilitate optimal care coordination and minimize time delay *.
      • Level I Center (cardiogenic shock center) is capable of PCI and implementation of MCS (short-term or long-term), and available on-site operating rooms with cardiothoracic surgery and a highly experienced multidisciplinary team (MDT).
      • Level II Centers have PCI available but usually do not have MCS.
    • All patients with CS should be rapidly transferred to a tertiary care center which has the service of cardiac catheterization, and a dedicated ICU/ICCU with availability of short-term MCS *.

    Medical Treatment

    The center of focus in this review is the management of florid cardiogenic shock typical of LV failure or biventricular failure. Medical treatment of CS in specific clinical conditions is discussed separately as:

    • Takotsubo Syndrome 📖, Dynamic LVOTO 📖.
    • SCAPE (Sympathetic Crashing Acute Pulmonary Edema) 📖.
    • RV failure: Principles of hemodynamic management 📖.
    • Valvular Emergencies: AS 📖, AR📖,MS 📖, MR📖.

    The overall view of the medical management of florid cardiogenic shock typical of LV failure or biventricular failure is shown below.

    Principles

    • Both RV and LV functions have to be improved since the heart consists of two pumps connected in series *.
    • A dynamic personalized therapeutic strategy should be employed *.
      • A “one-size-fits-all” approach to treating patients with CS does not account for individual treatment responsiveness and is not appropriate *.
    • There are 4 primary objectives in hemodynamic support of patients with CS, all of which should be achieved in a timely manner *.
      1. Circulatory support
        • Adequate circulatory support is defined by an increase in MAP and enhanced microvascular organ perfusion *.
        • Target: Generally, an initial MAP of 65-70 mmHg should be targeted *.
        • Monitoring the response to treatment: Improving functional markers of organ perfusion e.g. creatinine, urine output, and mental status is reassuring *. Down-trending lactate should be interpreted in the clinical context. More on this, here.
      2. Ventricular unloading
        • Defined as a reduction in myocardial work and wall stress, which is best achieved by reducing ventricular pressure and volume *.
        • Target: A 90 <SBP<120 mmHg; PCWP 10-18 *.
        • Monitoring the response to treatment: Resolving tachycardia (in the presence of improvement in organ perfusion), and down-trending BNP are reassuring *. Improving echocardiographic markers of (E/A, E/e’ ratio).
      3. Myocardial perfusion
        • See coronary perfusion pressure above.
          • Improving LV perfusion pressure (DBP-LVEDP) is achieved by increasing DBP and reducing LVEDP (LV preload).
          • Improving RV perfusion (MAP – MPAP) is achieved by raising MAP and reducing mean pulmonary artery pressure.
        • This is often associated with successful circulatory and ventricular support.
        • Monitoring the response to treatment: A down-trending cardiac troponin and resolving ST-T changes are reassuring *.
      4. Decongestion
        • Refers to a reduction in total body volume and elevated venous filling pressures, which is commonly associated with worsening renal function, hepatic failure, bowel edema, and subsequent sepsis *.
        • Target: A RAP 5-10 mm Hg, RAP/PCWP <0.86 *.
        • Monitoring the response to treatment: A down-trending serum creatinine, improving LFTs, coagulation profile *, decreasing IVC size, and increasing collapsibility are reassuring.
    • Limit the dose and the duration of vasoactive medications to the lowest possible dose when tissue perfusion is restored *.
      • Vasoactive medications may restore hemodynamics but they have significant shortcomings in many CS patients that render them inadequate. They will solve one part of the equation but at the cost of another, for example:
        • Vasopressors increase MAP but do not improve microvascular organ perfusion.
          • Increased MAP leads to increased LV afterload, resulting in increased myocardial work and wall stress promoting myocardial ischemia, impairing cardiac function, and increasing cardiac filling pressures.
          • In other words, vasopressors can increase BP, but typically at a cost of decreased CO and increased myocardial oxygen needs.
        • Inotropes have similar physiology which directly increase myocardial work and increase the likelihood of myocardial ischemia.
    • Mechanical circulatory support (MCS): The use of MCS has been increasingly advocated to circumvent the above shortcomings.

    Optimizing Lung Function

    Intubation

    • It is often required for frank CS (SCAI stage C) and multiorgan failure (e.g. delirium, renal failure).
    • It provides full support for the work of breathing, which may allow the shunting of blood away from the diaphragm and towards vital organs *.
      • The effects of positive pressure ventilation can vary (figure below) *.
    • ⚠️Intubation in CS carries risks of hypotension/arrest. It’s often safer to resuscitate them before intubation *.
    cardiogenic shock the effect of positive pressure ventilation

    BiPAP (non-invasive ventilation)

    • It has been shown that patients with respiratory distress due to heart failure respond well to BiPAP. This can be applied to patients with less severe forms of CS without change in mental status or organ failure (e.g. SCAI stage B).
    • The most important parameter is the expiratory pressure, which should be ramped up rapidly if possible.

    Pleural effusion drainage

    • Drainage of pleural effusion is indicated in patients with significant respiratory distress or hypoxemia who have large effusion(s). More on this, here.

    Inhaled pulmonary vasodilators

    • Inhaled epoprostenol or nitric oxide may be considered for an intubated patient with biventricular failure or severe hypoxemia. Physiological benefits include:
      1. Reduction in RV afterload may improve cardiac output among patients with right ventricular failure.
      2. Inhaled pulmonary vasodilators will improve “perfusion: ventilation matching” and thereby improve oxygen saturation.
    • Administration of an inhaled pulmonary vasodilator can worsen cardiogenic pulmonary edema in patients with biventricular failure as improving RV output will result in receiving more blood in the left ventricle thereby increasing the pulmonary capillary wedge pressure. However, in the intubated patient this generally isn’t a major problem.

    Optimize MAP and HR

    In the presence of multiple hemodynamic derangements, it is crucially important to identify whether the abnormal heart rate is the cause of instability (i.e. if the abnormal heart rate is the cause of hypoperfusion).

    Arrhythmia-CS

    • Identify if the abnormal HR is the cause of CS. This could be present if the heart rate lies in the extremes, such as
      • Non-sinus tachycardia > 170 bpm.
      • Atrial fibrillation with ventricular response > 150 bpm.
      • Bradycardia: e.g. HR <30 bpm.
    • If shock is caused by new-onset tachyarrhythmia (e.g. atrial fibrillation with ventricular response >>150), then reversion to sinus rhythm may be beneficial.
      • However, if the heart rate isn’t very high (e.g. AF with RVR <150) then be careful. Slowing down the heart rate may lead to deterioration of clinical condition.
    • If shock is caused or aggravated by severe bradycardia, this should be treated accordingly.
      • Low-dose epinephrine might be the first choice *. This can work as a bridge to pacing. More on this,👉 here.

    Optimizing The Mean Arterial Pressure (MAP

    Hypotension impairs coronary and end-organ perfusion and should be corrected promptly.

    • Optimal MAP
      • The optimal MAP differs from patient to patient, and the risks of hypoperfusion with lower MAPs must be balanced (and individualized) with the potentially deleterious impact of vasoactive agents on myocardial oxygen demand, ischemia, and arrhythmia associated with higher MAP targets *.
      • Often an ideal blood pressure will be in the low-normal range (e.g., MAP 60-65 mm Hg).
        • A higher MAP may be beneficial in previously hypertensive patients *.
    • First-line vasopressor: It should be selected based on the patient’s physiology.
      • Norepinephrine is widely recommended as a front-line agent for CS.
        • Norepinephrine will improve blood pressure, but there is a risk that excessive afterload drops the cardiac output.
      • Epinephrine (low dose) could be a reasonable choice for a patient with reduced ejection fraction, hypotension, and poor cardiac output.
        • Epinephrine can be a therapeutic alternative to the combination of dobutamine and norepinephrine *.
          • At a very low dose (e.g. 0-5 mcg/min) epinephrine acts as an inotrope with a neutral effect on systemic vascular resistance (SVR). However, unlike dobutamine, epinephrine doesn’t cause vasodilation. 
          • At low doses (e.g. 5-10 mcg/min) epinephrine works predominantly as an inotrope with minimal increase in SVR.
      • Vasopressin
        • It is a non-sympathomimetic vasoconstrictor agent that increases SVR and MAP but does not affect pulmonary vascular resistance.
        • Vasopressin increases systemic arterial pressure by specifically inhibiting the same intracellular enzymes responsible for the vasodilator action of milrinone and may be used to counteract vasodilatation caused by milrinone *.
        • Vasopressin may be helpful in patients with tachycardia or pulmonary hypertension.
        • In combination with milrinone, administration of vasopressin at low doses increased systolic pressure and allowed discontinuation or a decrease in catecholamine vasopressors *.
    • ⚠️Dopamine: Should be avoided.
      • In the SOAP II trial, the pre-defined subgroup analysis of CS patients showed that dopamine was associated with higher 28-day mortality and increased arrhythmia burden, compared with norepinephrine *.
      • In a propensity-matching-score analysis from the ESC HF Long-Term registry, dopamine was associated with worse short- and long-term outcomes compared with other inotropes and vasopressors *.

    Hypertension (or high-normal BPs) should be managed with afterload reduction.

    • In patients with evidence of poor perfusion who are normotensive or hypertensive, afterload reduction may improve cardiac output, decongest the lungs, and reduce the myocardial workload *.
    • Agent of choice: In the acute phase, a high-dose nitroglycerine infusion is the safest vasodilator.
    • High doses may be needed to achieve arterial vasodilation 👉 📖.
    • This should be titrated against the patient’s blood pressure. See appendix.
    vasopressors, inotropes, vasodilators

    Optimize volume status

    Fluid administration

    • Consider giving a fluid challenge (e.g. Ringer’s lactate 250 mL over 15–30 min) if the following conditions are met:
      • No evidence of pulmonary congestion (e.g. no B-lines on lung ultrasound).
      • The multidimensional hemodynamic assessment suggests true hypovolemia (no evidence of systemic congestion).
    • Fluid should be given in boluses of 250-500 ml fluid challenges, with careful determination of the effect on the patient. Avoid giving further fluid, if it is not causing clinical improvement.
    • Static hemodynamic parameters (e.g., CVP, PCWP) do not predict fluid responsiveness and should not be used as the primary determinant of fluid administration.

    Diuresis

    • Diuresis should be considered if all the following conditions are met:
      • Presence of significant pulmonary and/or systemic congestion *.
      • Multidimensional hemodynamic assessment suggests total body fluid overload.
    • Loop diuretics remain the cornerstone for the treatment of congestion in patients with heart failure. If patient is not responding well to furosemide, consider adding a thiazide diuretic (e.g., metolazone 5 mg q12hr-q24hr) *. More on this, 👉 here.

    Optimize contractility

    • The addition of an inotrope (dobutamine) is recommended with a class IIb/C recommendation, reflecting the paucity of data in this setting *.
      • Inotropes will cause a short-term improvement in hemodynamics. However, available evidence indicates that inotrope use is associated with worse outcomes *.
    • Inotropes should be used only if necessary, for the following indication:
      • Hypoperfusion with low-normal blood pressure (e.g. acute kidney injury with poor urine output despite all above resuscitative measures).
      • Hypotensive patients with cardiogenic pulmonary edema: In such patients, inotropes may be used with the goal of reducing the PCWP and decongesting the lungs.
    • Dobutamine or milrinone?
      • An RCT comparing dobutamine vs. milrinone in patients with cardiogenic shock found no difference between the two agents *.
      • Both agents may cause hypotension, so they shouldn’t be used in profoundly hypotensive patients. Thus, it’s generally preferable to raise the MAP first.
      • Dobutamine has a shorter half-life which makes it more easily titratable, which arguably makes it the preferred agent.
      • Milrinone has a longer half-life  (2.3 hours) making rapid titration impossible. Moreover, milrinone is renally cleared so it may exhibit erratic pharmacokinetics in shocked patients (e.g., accumulating unexpectedly if there is a reduction in renal function).
    • Levosimendan
      • The inotropic effect of levosimendan is the result of a combined effect from both calcium sensitization and selective and potent phosphodiesterase 3 inhibition.
      • It also reduces peripheral vascular resistance by inhibiting K + channels in vascular smooth muscle, inducing arterial and venous vasodilatation *.
      • It may be used in particular CS with
        • Acute RV failure or pulmonary hypertension (owing to its favorable effects on pulmonary vascular resistance)
        • CS patients already on chronic beta-blocker therapy * or for adrenergic cardiomyopathy *.

    Considerations

    • Blood transfusion is indicated to standard target >7 mg/dL or, in a patient with evidence of active myocardial ischemia a target of >8 mg/dL is warranted.
    • ⚠️β-blockers should be avoided in CS and should be held in patients with CS who were previously taking them *.
    • ⚠️Avoid using medications with negative inotropic effects (e.g. non-dihydropyridine calcium channel blockers) in patients with CS *.
    • ⚠️Avoid using nephrotoxic medications in CS.
    • ⚠️Avoid vasodilators (e.g. ACEIs, ARBs) in hypotensive patients with CS.

    Mechanical Circulatory Support (MCS)

    cardiogenic shock
    • Background
      • Temporary MCS (tMCS) has an emerging role in CS.
        • Early use of MCS in patients with CS refractory to fluid load and inotropes/vasopressors is recommended (IIb/C).
      • However, MCS is associated with significant complications, requires specialist multidisciplinary expertise for implantation and management, and high-quality evidence regarding outcomes is largely absent.
      • Role of tMCS. Depending on the context, MCS may play a variety of different roles *
        • Bridge to recovery.
        • Bridge to re-evaluation, ideally following resolution of multi-organ failure (“bridge to bridge”).
        • Bridge to a more durable platform (LVAD or transplantation)
    • Options include intra-aortic balloon pumps (IABP), percutaneous centrifugal pumps, and full veno-arterial ECMO (characteristic of MCS 👉appendix).
    • Factors involved in determining mechanical support device
      • Is support needed for the left ventricle, the right ventricle, or both? (figure below) *,*.
      • Ability to tolerate anticoagulation? This is required for both temporary & durable devices.
    • Absolute contra-indications for all types of temporary MCS (tMCS) *
      • Severe irreversible noncardiac organ failure limiting survival (e.g. severe anoxic brain injury or metastatic cancer).
      • Irreversible cardiac failure if transplantation or long-term ventricular assist device (VAD) is not an option.
    • Relative contra-indications for all types of tMCS *
      • Moderate to severe aortic regurgitation.
      • Severe coagulopathy or contraindication to anticoagulation, including advanced liver disease.
      • Limited vascular access.
      • Aortic dissection, aneurysm, or severe atherosclerosis.
      • Advanced age.
      • Prolonged CPR >45 min.

    Intra-aortic balloon pumps (IABP)

    • The most popular devices overall and the most thoroughly investigated. However, RCTs fail to show improvement in patient-centered outcomes *,*.
    • The IABP produces a modest increase in CO of 0.5–1 L/min and may have even less benefit in patients with tachycardia and irregular rhythms *.
    • Contraindications *
      • Aortic dissection
      • Abdominal aortic aneurysm
      • Tachyarrhythmias

    Impella

    • Impella is a microaxial pump giving only left-sided support that unloads the left ventricle by expelling blood flow from the LV into the aorta and may provide up to >5 L/min of blood flow depending on the device used and depending on afterload.
    • Although it provides superior hemodynamic support compared to IABP, Impella failed to show any difference when compared to an intra-aortic balloon pump AMI-CS *.
    • A recent retrospective registry study compared matched patients treated with Impella vs. IABP showed that patients treated with Impella had some improvement in renal function, more bleeding, and more peripheral vascular complications, but no difference in mortality *.
    • Contraindications *
      • LV thrombus.
      • Severe aortic stenosis is a consideration, but if the valve can be crossed with a wire is not an absolute contraindication.
        Mechanical aortic valve.
        Aortic dissection.
      • Ventricular septal defect (VSD) *

    TandemHeart

    • It provides a continuous flow (4 L/min) via a centrifugal pump.
    • In two randomized studies, including AMI-CS patients, TandemHeart significantly improved hemodynamic indices as compared to IABP, but 30-day mortality did not differ between the two groups *,*.
    • Contra-indication: Intra-atrial thrombus *

    Venous-arterial ECMO

    • It provides cardiopulmonary support by draining venous blood from the right atrium and returning it after oxygenation to the ascending aorta (central cannulation) or to the iliac artery (peripheral cannulation).
    • V-A ECMO provides high levels of biventricular cardiac (V-A) and respiratory support (V-V) in a large spectrum of clinical settings, including CS patients with malignant arrhythmias and CA *.
    • Contra-indication: Aortic dissection (if peripheral cannulation) *

    Post-tMCS monitoring

    • The principles of in-hospital patient evaluation and monitoring were discussed earlier.
    • Of note, echocardiography plays a potential role in monitoring patients with transient mechanical circulatory support. See appendix.

    Etiologic treatment

    Early identification and treatment of the underlying etiology of CS is potentially beneficial in improving outcomes *. The general principles of CS management and Heart Team activation are presented in the following figure *.

    • Non-ACS etiologies of CS. The treatment is discussed separately (for a summary of treatment principles of patients with non-ACS CS, see the appendix). 
      • See more: Pulmonary embolism 📖, tamponade 📖, β-blocker and calcium channel blocker intoxication 📖.
    • AMI-CS
      • In patients with ACS in cardiogenic shock, early revascularization strategy is the cornerstone in the management *,*. More on this, here.
        • Revascularization is essential. This is beneficial even at delayed time points.
        • Thrombolysis works poorly in CS. PCI or CABG is generally necessary.
          • PCI strategy: Early culprit vessel revascularization is recommended. 
          • Patients with acute myocardial infarction (AMI) with cardiogenic shock frequently have multiple vessel disease.
          • The CULPRIT-SHOCK trail Among patients who had multivessel coronary artery disease and AMI with cardiogenic shock, the 30-day risk of a composite of death or severe renal failure leading to renal-replacement therapy was lower among those who initially underwent PCI of the culprit lesion only than among those who underwent immediate multivessel PCI *.

    Media

    Normotensive Cardiogenic Shock

    Lung Ultrasound: Profiles

    Going further

    Appendix

    Pathophysiology of cardiogenic shock with staged abnormalities of clinic examination

    Potential challenges in using echocardiography to determine the underlying cause of AHF

    Proposed initial focused cardiac and lung ultrasonography assessment for patients with suspected AHF in acute care settings

    Pulmonary artery catheter hemodynamic data

    Management of SCAPE

    Characteristics of mechanical circulatory supports

    Echocardiography for acute mechanical circulatory support

    Management of non-acute coronary syndrome etiologies of cardiogenic shock

    References

    Expand to view the reference list

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    I am Shahriar Lahouti and RECAP EM is my primary FOAMed project. The philosophy of RECAP EM is to promote critical thinking and enlightening the mindsets with most rational, current evidence towards a safer practice.

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