Cardiogenic Shock

Etiology

Arrhythmia/Conduction Disturbance

Bradyarrhythmia
- Second Degree Atrioventricular Block-Mobitz Type II (Second Degree Heart Block-Mobitz Type II) (see Second Degree Atrioventricular Block-Mobitz Type II)
- Sinus Bradycardia/Sinus Pauses/Sinus Arrest (see Sinus Bradycardia)
  - Sinus Node Dysfunction (see Sinus Node Dysfunction)
- Third Degree Atrioventricular Block (Third Degree Heart Block, Complete Heart Block) (see Third Degree Atrioventricular Block)
Tachyarrythmia
- Atrial Fibrillation/Flutter (see Atrial Fibrillation): particularly with rapid ventricular response
- Supraventricular Tachycardia (SVT) (see Supraventricular Tachycardia): notably at high ventricular rates
- Ventricular Fibrillation (see Ventricular Fibrillation)
- Ventricular Tachycardia (VT) (see Ventricular Tachycardia)

Cardiomyopathy (see Congestive Heart Failure)

Primary Cardiomyopathies (Predominantly Involving the Heart)
Secondary Cardiomyopathies

Increased Afterload

Aortic Coarctation (see Aortic Coarctation)
- Epidemiology
  - Congenital: most cases
  - Acquired: few cases
- Physiology
  - Narrowing of Descending Aorta (Typically at the Insertion of the Ductus Arteriosus Distal to the Left Subclavian Artery), Resulting in Left Ventricular Pressure Overload
Malignant Hypertension (see Hypertension)
- Physiology
  - Left Ventricular Pressure Overload

Valvular Heart Disease/Cardiac Mechanical Disturbance/Intracardiac Shunt

Aortic Insufficiency (AI) (see Aortic Insufficiency)
- Epidemiology
  - Aortic Insufficiency May Be Acute in the Setting of Ascending Aortic Dissection
- Physiology
  - Portion of Left Ventricular Stroke Volume Regurgitates Back from the Aorta into the Left Ventricle, Resulting in Increased Left Ventricular End-Diastolic Volume and Increased Left Ventricular Wall Stress
Aortic Stenosis (AS) (see Aortic Stenosis)
- Physiology
  - Increased Left Ventricular Afterload
Atrial Myxoma (see Atrial Myxoma)
- Physiology
  - Symptomatic Left Atrial Tumors Typically Result in Obstruction to Blood Flow, Mitral Regurgitation, and/or Systemic Embolization
Atrial Septal Defect (ASD) (see Atrial Septal Defect)
- Physiology
  - Left-to-Right or Right-to-Left Intracardiac Shunt
Atrial Thrombus (see Intracardiac Thrombus)
- Physiology
  - May Result in Systemic Embolization (or Less Commonly, Obstruction to Blood Flow)
Constrictive Pericarditis (see Constrictive Pericarditis)
- Physiology
  - Early Diastolic Ventricular Filling is More Rapid Than Normal
  - However, Starting in Mid-Diastole, Inelastic Pericardium Results in Compression, Impairing Further Ventricular Filling and Compromising Stroke Volume
Hypertrophic Obstructive Cardiomyopathy (HOCM) (see Hypertrophic Cardiomyopathy)
- Physiology
  - Left Ventricular Outflow Tract Obstruction
Left Ventricular Aneurysm (see Left Ventricular Aneurysm)
- Physiology
  - Bulging of Left Ventricular Wall, Resulting in Decreased Stroke Volume
  - In Rare Cases Where Left Ventricular Aneurysm Rupture Occurs, Tamponade May Occur
Left Ventricular Pseudoaneurysm (see Left Ventricular Pseudoaneurysm)
- Physiology
  - Cardiac Rupture is Contained by Adherent Pericardium or Scar Tissue (Pseudoaneurysm Contains No Endocardium or Myocardium), Resulting in Decreased Stroke Volume
  - In Cases Where Left Ventricular Pseudoaneurysm Rupture Occurs, Tamponade May Occur
Left Ventricular Thrombus (see Left Ventricular Thrombus)
- Physiology
  - May Result in Systemic Embolization (or Less Commonly, Obstruction to Blood Flow)
Mitral Regurgitation (MR) (see Mitral Regurgitation)
- Epidemiology
  - Mitral Regurgitation May Be Acute in the Setting of Myocardial Infarction-Associated Papillary Muscle Dysfunction/Rupture or Chordae Tendineae Rupture
- Physiology
  - Decreased Effective Forward Flow
Mitral Stenosis (see Mitral Stenosis)
- Physiology
  - Impaired Left Ventricular Filling
Pulmonic Stenosis (see Pulmonic Stenosis)
- Physiology
  - Right Ventricular Pressure Overload
Restrictive Cardiomyopathy (see Congestive Heart Failure)
- Physiology
  - Diastolic Dysfunction (Restricted Filling)
Ruptured Sinus of Valsalva Aneurysm (see Sinus of Valsalva Aneurysm)
- Physiology
  - May Produce Aortic Insufficiency, Tricuspid Regurgitation, Left-to-Right or Right-to-Left Shunt, and/or Sudden Cardiac Death
Tamponade (see Tamponade)
- Physiology
  - Diastolic Dysfunction
Tricuspid Regurgitation (TR) (see Tricuspid Regurgitation)
- Physiology
  - Right Ventricular Pressure/Volume Overload, Resulting in Right Ventricular Systolic Dysfunction
Tricuspid Stenosis (see Tricuspid Stenosis)
- Physiology
  - Impaired Right Ventricular Filling
Ventricular Septal Defect (VSD) (see Ventricular Septal Defect)
- Physiology
  - Left-to-Right or Right-to-Left Intracardiac Shunt
Ventricular Septal Rupture (see Ventricular Septal Rupture)
- Physiology
  - Left-to-Right or Right-to-Left Intracardiac Shunt

Obstructive Shock (Cardiac Pump Failure Due to an Extracardiac Etiology)

Mechanical

Abdominal Compartment Syndrome (see Abdominal Compartment Syndrome)
- Physiology
  - Decreased Venous Return to Right Side of Heart
  - Impaired Myocardial Contractility
Aortocaval Compression (Due to Positioning or Surgical Retraction)
- Physiology
  - Caval Compression, Resulting in Decreased Venous Return to Right Side of Heart
  - Aortic Compression, Resulting in Increased Left Ventricular Afterload
Dynamic Hyperinflation (Severe)
- Positive End-Expiratory Pressure (PEEP)/Auto-PEEP (see Invasive Mechanical Ventilation-General)
  - Physiology
    - Increased Intrathoracic Pressure, Resulting in Decreased Venous Return to Right Side of Heart
Hemothorax (Large) (see Pleural Effusion-Hemothorax)
- Physiology
  - Increased Intrathoracic Pressure with Mass Effect on the Mediastinum (with Compression of Heart and Great Vessels) and the Contralateral Lung
Herniation of Abdominal Viscera Into the Thorax
- Physiology
  - Increased Intrathoracic Pressure, Resulting in Decreased Venous Return to the Right-Side of the Heart
Positive-Pressure Ventilation with High Airway Pressures (see Acute Respiratory Distress Syndrome)
- Physiology
  - Increased Intrathoracic Pressure, Resulting in Decreased Venous Return to the Right Side of Heart
Tension Pneumothorax (see Pneumothorax)
- Physiology
  - Increased Intrathoracic Pressure with Mass Effect on the Mediastinum (with Compression of Heart and Great Vessels) and the Contralateral Lung

Pulmonary Vascular

Acute or Severe Pulmonary Hypertension (see Pulmonary Hypertension)
- General Comments: abrupt/severe increase in pulmonary pressure (i.e. increased pulmonary vascular resistance) results in right-sided heart failure (which may subsequently impair left ventricular filling)
- Acute Pulmonary Embolism (PE) (see Acute Pulmonary Embolism)
  - Physiology
    - Mechanical Obstruction of Pulmonary Vasculature by Embolism
    - Pulmonary Vasoconstriction (Due to Release of Serotonin and Thromboxane) (Cardiovascular Res, 2000) [MEDLINE]
- Chronic Thromboembolic Pulmonary Hypertension (CTEPH) (see Chronic Thromboembolic Pulmonary Hypertension)
  - Physiology
    - Mechanical Obstruction of Pulmonary Vasculature
- Idiopathic Pulmonary Arterial Hypertension (IPAH) (see Idiopathic Pulmonary Arterial Hypertension)
  - Physiology
    - Pulmonary Vascular Smooth Muscle Proliferation and Vasoconstriction
- Other Causes of Severe Pumonary Hypertension
Venous Air Embolism (see Air Embolism)
- Physiology
  - Venous Air Embolized to the Pulmonary Vasculature in a Sufficient Amount to Obstruct Pulmonary Arterial Blood Flow

Diagnosis

Echocardiogram: usually diagnostic
Swan
- Cardiac Output (CO): usually decreased
- Increased Extraction Ratio (Decreased SvO2): in cases with decreased CO

Clinical

Hypotension (see Hypotension)
Pulseless Electrical Activity (PEA) (see Pulseless Electrical Activity): may occur in cases of tension pneumothorax, tamponade

Treatment

Inotropes

Norepinephrine: improves myocardial oxygen metabolism (increases myocardial lactate extraction) in patients with cardiogenic shock by increasing perfusion pressure and myocardial oxygen supply
Dopamine: worsens myocardial oxygen metabolism because of the associated tachycardia
- In cardiogenic shock, the use of dopamine increases mortality, as compared to norepinephrine

Clinical Efficacy

Comparison of Dopamine with Norepinephrine in Shock of Various Etiologies (NEJM, 2010) [MEDLINE]: in shock, there was no difference in mortality rate between dopamine and norepinephrine
- However, Dopamine Was Associated with More Arrhythmic Adverse Events
- Use of Additional Vasopressin and Epinephrine for Unresponsive Shock was Similar in Both Groups
- In Subgroup with Cardiogenic Shock, Dopamine Increased 28-Day Mortality, as Compared to Norepinephrine: this increase in mortality was not observed in septic and hypovolemic shock

Intra-Aortic Balloon Pump (IABP)

Useful for cases unresponsive to medical therapy
Inflates during early diastole (pushing blood toward head and neck arteries and coronary arteries) with rapid deflation prior to systole: decreased afterload (decreased SVR)/ decreased LV-EDP/ modestly decreased aortic systolic pressure -> increased CO
- In cases of MR or VSD, aortic systolic pressure usually increases modestly
Improves myocardial lactate production, arterial BP, and CO
Proven to improve survival only in MI patients with complicating ruptured ventricular septum or ruptured papillary muscle

Packed Red Blood Cell (PRBC) Transfusion

No specific Hct has been documented to improve any clinical factor or outcome
However, doubling the Hct (from 20 to 40%) will double plasma viscosity, increasing O2 delivery to coronary arteries but increasing myocardial work

References

Effect of isoproterenol, norepinephrine and intraaortic counterpulsation on hemodynamics and myocardial metabolism in shock following myocardial infarction. Circulation 1972; 37:335- 351
Effect of dopamine on hemodynamics and myocardial metabolism in shock following acute myocardial infarction in man. Circulation 1978; 57:361-365
Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med 2010; 362:779-789 [MEDLINE]