Etiology
Cardiogenic Shock (see Cardiogenic Shock)
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 (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 (see Atrial Fibrillation): particularly with rapid ventricular response
- Atrial Flutter (see Atrial Flutter): particularly with rapid ventricular response
- Supraventricular Tachycardia (SVT) (see Supraventricular Tachycardia)
- Ventricular Fibrillation (see Ventricular Fibrillation)
- Ventricular Tachycardia (VT) (see Ventricular Tachycardia)
Cardiomyopathy (see Congestive Heart Failure)
- Primary Cardiomyopathies (Predominantly Involving the Heart)
- Genetic
- Arrhythmogenic Right Ventricular Cardiomyopathy (Arrhythmogenic Right Ventricular Dysplasia) (see Arrhythmogenic Right Ventricular Cardiomyopathy)
- Conduction System Disease
- Lenegre Disease
- Sinus Node Dysfunction (see Sinus Node Dysfunction)
- Glycogen Storage Diseases
- Danon
- PRKAG2
- Hypertrophic Cardiomyopathy
- Ion Channelopathies
- Brugada Syndrome
- Catecholaminergic Polymorphic Ventricular Tachycardia
- Idiopathic Ventricular Fibrillation
- Long-QT Syndrome
- Short-QT Syndrome
- Left Ventricular Noncompaction
- Mitochondrial Myopathies
- Mixed (Predominantly Non-Genetic; Familial Disease with a Genetic Origin has been Reported in a Minority of Cases)
- Dilated Cardiomyopathy: this is a heterogeneous group of disorders characaterized by ventricular dilation and decreased myocardial contractility in the absence of abnormal loading (valvular heart disease, hypertension)
- Restrictive Cardiomyopathy (Non-Dilated and Non-Hypertrophied)
- Acquired
- Cardiomyopathy in Infants of Insulin-Dependent Diabetic Mothers
- Myocarditis (Inflammatory Cardiomyopathy) (see Myocarditis)
- Peripartum Cardiomyopathy
- Tachycardia-Induced Cardiomyopathy
- Takotsubo Cardiomyopathy (Stress Cardiomyopathy) (see Takotsubo Cardiomyopathy)
- Genetic
- Secondary Cardiomyopathies
- Cardiofacial
- Lentiginosis
- Noonan Syndrome
- Endocrine/Metabolic
- Acidosis (see Metabolic Acidosis-General)
- Acromegaly (see Acromegaly)
- Diabetes Mellitus (see Diabetes Mellitus)
- Growth Hormone Deficiency: growth hormone and insulin-like growth factor 1 and required for cardiac development
- Hyperparathyroidism (see Hyperparathyroidism)
- Hyperthyroidism (see Hyperthyroidism)
- Hypocalcemia (see Hypocalcemia)
- Hypokalemia (see Hypokalemia)
- Hypophosphatemia (see Hypophosphatemia)
- Hypothyroidism (see Hypothyroidism)
- Hypoxia (see Hypoxemia)
- Obesity (see Obesity)
- Pheochromocytoma (see Pheochromocytoma)
- Endomyocardial
- Endomyocardial Fibrosis
- Hypereosinophilic Syndrome (Löeffler’s Endocarditis????)(see Hypereosinophilic Syndrome)
- Hematologic Disease
- Sickle Cell Disease (see Sickle Cell Disease)
- Anemia (see Anemia)
- Henoch-Schonlein Purpura (see Henoch-Schonlein Purpura)
- Infectious/Inflammatory
- Hantavirus Cardiopulmonary Syndrome (see Hantavirus Cardiopulmonary Syndrome): unusually produces sepsis with a low CO and high SVR physiology
- Hantavirus Genus: Sin Nombre Virus (SNV) is the most commonly associated Hantavirus in the US
- Hemorrhagic Fever with Renal Syndrome (HFRS) (see Hemorrhagic Fever with Renal Syndrome)
- Hantavirus Genus: Hantaan Virus, Dobrova Virus, Seoul Virus (Baltimore Rat Virus)
- Sarcoidosis (see Sarcoidosis)
- Sepsis-Induced Myocardial Depression (see Sepsis)
- Hantavirus Cardiopulmonary Syndrome (see Hantavirus Cardiopulmonary Syndrome): unusually produces sepsis with a low CO and high SVR physiology
- Infiltrative (Accumulation of Abnormal Substances in Extracellular Space Between Myocytes)
- Amyloidosis (see Amyloidosis)
- Gaucher’s Disease
- Hunter’s Syndrome
- Hurler’s Syndrome
- Ischemic
- Acute Myocardial Infarction (MI) (see Coronary Artery Disease)
- Physiology: involving >40% of left ventricular myocardium or right ventricular infarction
- Myocardial Ischemia
- Stunned Myocardium (from Prolonged Ischemia)
- Cardiac Arrest (see Cardiac Arrest)
- Post-Cardiopulmonary Bypass (CPB) (see Cardiopulmonary Bypass)
- Prolonged Hypotension
- Acute Myocardial Infarction (MI) (see Coronary Artery Disease)
- Neoplasm
- Leukemia
- Multiple Myeloma (see Multiple Myeloma)
- Neuromuscular/Neurologic
- Becker Muscular Dystrophy (see Becker Muscular Dystrophy)
- Chronic Progressive External Opthmoplegia (Kearns-Savre)
- Duchenne Muscular Dystrophy (see Duchenne Muscular Dystrophy)
- Emery-Dreifuss Muscular Dystrophy
- Familial Centronuclear Myopathy
- Fascioscapulohumeral Dystrophy (Landouzy-Dejerine)
- Friedrich’s Ataxia
- Humuloperitoneal Ataxia
- Juvenile Progressive Spinal Muscular Atrophy (Kugelberg-Welander)
- Limb-Girdle Muscular Dystrophy
- Myotonia Atrophica (Steinert)
- Myotonic Dystrophy
- Neurofibromatosis (see Neurofibromatosis)
- Tuberous Sclerosis (see Tuberous Sclerosis)
- Nutritional
- Rheumatologic
- Behcet’s Disease (see Behcet’s Disease)
- Eosinophilic Granulomatosis with Polyangiitis (EGPA, Churg-Strauss Syndrome) (see Eosinophilic Granulomatosis with Polyangiitis)
- Granulomatosis with Polyangiitis (GPA, Wegener’s Granulomatosis) (see Granulomatosis with Polyangiitis)
- Microscopic Polyangiitis (see Microscopic Polyangiitis)
- Polyarteritis Nodosa (PAN) (see Polyarteritis Nodosa)
- Polydermatomyositis (see Polydermatomyositis)
- Rheumatoid Arthritis (RA) (see Rheumatoid Arthritis)
- Scleroderma (see Scleroderma)
- Systemic Lupus Erythematosus (SLE) (see Systemic Lupus Erythematosus)
- Storage (Accumulation of Abnormal Substances Intracellularly Within Myocytes)
- Fabry’s Disease
- Hemochromatosis (see Hemochromatosis)
- Niemann-Pick Disease
- Ochronosis
- Oxalosis (see Primary Hyperoxaluria)
- Pompe’s Disease
- Traumatic
- Cardiac Contusion (see Cardiac Contusion)
- Drug/Toxin
- 5-Fluorouracil (5-FU) (see 5-Fluorouracil)
- Amiodarone (see Amiodarone)
- Pharmacology: negative inotropy can occur in patients with preexisting left ventricular dysfunction with EF <35% (amiodarone also casuses peripheral vasodilation, which may offset some of the negative inotropy)
- Amphetamine (see Amphetamine)
- Anabolic Steroids (see xxxx)
- Antimalarials
- Chloroquine (Aralen) (see Chloroquine)
- Hydroxychloroquine (Plaquenil) (see Hydroxychloroquine)
- Antimony (see Antimony)
- Antracyclines
- Daunorubicin (Daunomycin, Cerubidine) (see Daunorubicin)
- Doxorubicin (Adriamycin) (see Doxorubicin)
- Arsenic (see Arsenic)
- β-Blocker Intoxication (see β-Adrenergic Receptor Antagonists)
- Pharmacology: negative inotropy may particularly occur in the setting of intoxication
- Calcium Channel Blocker Intoxication (see Calcium Channel Blockers)
- Pharmacology: negative inotropy may particularly occur in the setting of intoxication
- Carboxyhemoglobinemia (see Carboxyhemoglobinemia)
- Carbon Tetrachloride (see Carbon Tetrachloride)
- Catecholamines
- Clozapine (Clozaril) (see Clozapine)
- Cobalt (see Cobalt)
- Cocaine (see Cocaine)
- Cyclophosphamide (Cytoxan) (see Cyclophosphamide)
- Emetine(see Emetine)
- Ephedra (see Ephedra)
- Ethanol (see Ethanol)
- Hydrocarbon Intoxication (see Hydrocarbons)
- Interferons (see Interferons)
- Lead (see Lead)
- Lithium (see Lithium)
- Mercury (see Mercury)
- Methamphetamine (see Methamphetamine)
- Acute Methamphetamine Intoxication
- Chronic Methamphetamine Abuse
- Methylphenidate (Ritalin) (see Methylphenidate)
- Methysergide (see Methysergide)
- Mitomycin-C (see Mitomycin)
- Phenothiazines (se Phenothiazines)
- Propofol Infusion Syndrome (see Propofol)
- Taxanes (see Taxanes)
- Docetaxel (Taxotere) (see Docetaxel)
- Paclitaxel (Taxol) (see Paclitaxel)
- Trastuzumab (Herceptin) (see Trastuzumab)
- Tricyclic Antidepressants (see Tricyclic Antidepressants)
- White Phosphorus Toxicity (see White White Phosphorus)
- Widow Spider Bite (see Widow Spider Bite): cardiomyopathy occurs rarely
- Zidovudine (Retrovir) (see Zidovudine)
- Other
- Radiation Therapy (see Radiation Therapy)
- Stiff Left Atrial Syndrome Following Left Atrial Catheter Ablation (see Stiff Left Atrial Syndrome)
- Epidemiology: XXXX
- Physiology: XXXX
- Cardiofacial
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
- Epidemiology
- Hypertrophic Obstructive Cardiomyopathy (HOCM) (see Hypertrophic Cardiomyopathy)
- Malignant Hypertension (see Hypertension)
- Physiology
- Left Ventricular Pressure Overload
- Physiology
- Severe Aortic Stenosis (see Aortic Stenosis)
Intracardiac Shunt
- Atrial Septal Defect (ASD) (see Atrial Septal Defect)
- Physiology
- Left-to-Right or Right-to-Left Intracardiac Shunt
- Physiology
- Ruptured Sinus of Valsalva Aneurysm (see Sinus of Valsalva Aneurysm)
- Physiology
- Ruptured Sinus of Valsalva Aneurysm May Produce Aortic Insufficiency, Tricuspid Regurgitation, Left-to-Right or Right-to-Left Shunt, and/or Sudden Cardiac Death
- Physiology
- Ventricular Septal Defect (VSD) (see Ventricular Septal Defect)
- Physiology
- Left-to-Right or Right-to-Left Intracardiac Shunt
- Physiology
- Ventricular Septal Rupture (see Ventricular Septal Rupture)
- Physiology
- Left-to-Right or Right-to-Left Intracardiac Shunt
- Physiology
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
- Epidemiology
- Aortic Stenosis (AS) (see Aortic Stenosis)
- Physiology
- Increased Left Ventricular Afterload
- Physiology
- Atrial Myxoma (see Atrial Myxoma)
- Physiology
- Symptomatic Left Atrial Tumors Typically Result in Obstruction to Blood Flow, Mitral Regurgitation, and/or Systemic Embolization
- Physiology
- Atrial Septal Defect (ASD) (see Atrial Septal Defect)
- Physiology
- Left-to-Right or Right-to-Left Intracardiac Shunt
- Physiology
- Atrial Thrombus (see Intracardiac Thrombus)
- Physiology
- May Result in Systemic Embolization (or Less Commonly, Obstruction to Blood Flow)
- Physiology
- 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
- Physiology
- Hypertrophic Obstructive Cardiomyopathy (HOCM) (see Hypertrophic Cardiomyopathy)
- Physiology
- Left Ventricular Outflow Tract Obstruction
- Physiology
- 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
- Physiology
- 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
- Physiology
- Left Ventricular Thrombus (see Left Ventricular Thrombus)
- Physiology
- May Result in Systemic Embolization (or Less Commonly, Obstruction to Blood Flow)
- Physiology
- 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
- Epidemiology
- Mitral Stenosis (see Mitral Stenosis)
- Physiology
- Impaired Left Ventricular Filling
- Physiology
- Pulmonic Stenosis (see Pulmonic Stenosis)
- Physiology
- Right Ventricular Pressure Overload
- Physiology
- Restrictive Cardiomyopathy (see Congestive Heart Failure)
- Physiology
- Diastolic Dysfunction (Restricted Filling)
- Physiology
- 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
- Physiology
- Tamponade (see Tamponade)
- Physiology
- Diastolic Dysfunction
- Physiology
- Tricuspid Regurgitation (TR) (see Tricuspid Regurgitation)
- Physiology
- Right Ventricular Pressure/Volume Overload, Resulting in Right Ventricular Systolic Dysfunction
- Physiology
- Tricuspid Stenosis (see Tricuspid Stenosis)
- Physiology
- Impaired Right Ventricular Filling
- Physiology
- Ventricular Septal Defect (VSD) (see Ventricular Septal Defect)
- Physiology
- Left-to-Right or Right-to-Left Intracardiac Shunt
- Physiology
- Ventricular Septal Rupture (see Ventricular Septal Rupture)
- Physiology
- Left-to-Right or Right-to-Left Intracardiac Shunt
- Physiology
Obstructive Shock (Cardiac Pump Failure Due to an Extracardiac Etiology)
Mechanical
- Aortocaval Compression (Due to Positioning or Surgical Retraction)
- Physiology
- Compression of Aorta, Resulting in Increased Afterload
- Compression of Inferior Vena Cava, Resulting in Impaired Right-Sided Venous Return
- Physiology
- Increased Intrathoracic Pressure (with Impaired Right-Sided Venous Return)
- Abdominal Compartment Syndrome (see Abdominal Compartment Syndrome)
- Physiology
- Increased Intraabdominal Pressure, Resulting in Transmission with Intrathoracic Pressure, Culminating in Impaired Right-Sided Venous Return
- Increased Intraabdominal Pressure, Resulting in Impaired Right-Sided Venous Return
- Increased Intraabdominal Pressure, Resulting in Increased Afterload
- Physiology
- Dynamic Hyperinflation Associated with High Positive End-Expiratory Pressure (PEEP)/Auto-PEEP (see PEEP + Auto-PEEP)
- Physiology
- Increased Intrathoracic Pressure, Resulting in Impaired Right-Sided Venous Return
- Physiology
- Hemothorax (see Pleural Effusion-Hemothorax)
- Physiology
- Increased Intrathoracic Pressure, Resulting in Impaired Right-Sided Venous Return
- Physiology
- Herniation of Abdominal Viscera Into Thorax
- Physiology
- Due to Movement of Abdominal Visceral Contents into the Thoracic Cavity, there is Increased Intrathoracic Pressure, Resulting in Impaired Right-Sided Venous Return
- Physiology
- Positive-Pressure Ventilation with High Airway Pressures (see Acute Respiratory Distress Syndrome)
- Physiology
- Increased Intrathoracic Pressure, Resulting in Impaired Right-Sided Venous Return
- Physiology
- Tension Pneumothorax (see Pneumothorax
- Physiology
- Increased Intrathoracic Pressure, Resulting in Impaired Right-Sided Venous Return
- Physiology
- Abdominal Compartment Syndrome (see Abdominal Compartment Syndrome)
Pulmonary Vascular
- Acute or Severe Pulmonary Hypertension (see Pulmonary Hypertension)
- General Comments: typically causes right-sided heart failure
- Acute Pulmonary Embolism (PE) (see Acute Pulmonary Embolism)
- Chronic Thromboembolic Pulmonary Hypertension (CTEPH) (see Chronic Thromboembolic Pulmonary Hypertension)
- Idiopathic Pulmonary Arterial Hypertension (IPAH) (see Idiopathic Pulmonary Arterial Hypertension)
- Other Causes of Severe Pumonary Hypertension
- Venous Air Embolism (see Air Embolism)
Distributive Shock (Vasodilatory Shock)
Anaphylaxis/Anaphylactic Shock
- Anaphylaxis (see Anaphylaxis)
- Physiology
- Peripheral Vasodilation (Due to Histamine and Other Vasoactive Substances)
- Physiology
Infection
- Anaplasmosis Sepsis-Like or Toxic Shock-Like Syndrome (see Anaplasmosis)
- Ehrlichiosis Sepsis-Like or Toxic Shock-Like Syndrome (see Ehrlichiosis)
- Sepsis/Septic Shock (see Sepsis)
- Epidemiology
- Sepsis is the Most Common Etiology of Distributive Sshock
- Physiology
- Third-Spacing of Fluids (with Decreased Intravascular Volume) and Peripheral Vasodilation
- Epidemiology
- Toxic Shock Syndrome (TSS)
- Types
- Staphylococcal Toxic Shock Syndrome (see Staphylococcal Toxic Shock Syndrome)
- Streptococcal Toxic Shock Syndrome (see Streptococcal Toxic Shock Syndrome)
- Physiology
- Peripheral Vasodilation
- Types
Systemic Inflammatory Response Syndrome (SIRS) (see Sepsis)
- Acute Pancreatitis (see Acute Pancreatitis)
- Physiology
- Third-Spacing of Fluids (with Decreased Intravascular Volume) and Peripheral Vasodilation
- Physiology
- Air Embolism (see Air Embolism)
- Physiology
- XXXXXXX
- Physiology
- Amniotic Fluid Embolism (see Amniotic Fluid Embolism)
- Burns (see Burns)
- Crush Injury
- Fat Embolism (see Fat Embolism)
- Idiopathic Systemic Capillary Leak Syndrome (see Idiopathic Systemic Capillary Leak Syndrome)
- Post-Cardiac Arrest with Return of Spontaneous Circulation (see Cardiac Arrest)
- Trauma (see Trauma-General)
Endocrine/Metabolic/Nutritional Deficiency-Associated Hypotension
- Acidemia
- Metabolic Acidosis-Elevated Anion Gap (see Metabolic Acidosis-Elevated Anion Gap)
- Physiology
- XXXXX
- Physiology
- Metabolic Acidosis-Normal Anion Gap (see Metabolic Acidosis-Normal Anion Gap)
- Physiology
- XXXX
- Physiology
- Metabolic Acidosis-Elevated Anion Gap (see Metabolic Acidosis-Elevated Anion Gap)
- Adrenal Insufficiency (see Adrenal Insufficiency)
- Physiology
- Peripheral Vasodilation
- Physiology
- Hyperthyroidism (see Hyperthyroidism)
- Physiology
- XXXX
- Physiology
- Hypocalcemia (see Hypocalcemia)
- Epidemiology
- Cases of Hypocalcemia-Associated Hypotension Have Been Extensively Reported (Am J Kidney Dis, 1994) [MEDLINE] (Am J Kidney Dis, 2015) [MEDLINE] (Hemodial Int, 2016) [MEDLINE]
- Hypocalcemia-Associated Hypotension is Most Commonly Seen When it is Rapidly Induced by Ethylenediaminetetraacetic Acid (EDTA), Transfusion of Citrated Blood, Products, or with the Use of Low Calcium Dialysate in Patients Undergoing Dialysis
- Epidemiology
- Hypothyroidism/Myxedema (see Hypothyroidism)
- Physiology
- Peripheral Vasodilation
- Physiology
- Pheochromocytoma (see Pheochromocytoma)
- Epidemiology
- Occurs in Some Cases
- Clinical Patterns
- Episodic Hypotension: in rare cases where the tumor secretes only epinephrine
- Pattern of Rapid Cyclic Fluctuation Between Hypertension and Hypotension (Cycling Every 7-15 min): unclear mechanism
- Orthostatic Hypotension: due predominantly to decreased plasma volume
- Epidemiology
- Thiamine Deficiency (Beriberi) (see Thiamine)
- Physiology
- Peripheral Vasodilation
- Physiology
Hematologic Disease-Associated Hypotension
- Acute Graft vs Host Disease (see Graft vs Host Disease)
- Acute Hemolytic Transfusion Reaction (see Acute Hemolytic Transfusion Reaction)
- Severe Chronic Anemia (see Anemia)
- Physiology
- XXXXXXX
- Physiology
Neurogenic Shock (see Neurogenic Shock)
- Acute Spinal Cord Injury (SCI) (see Acute Spinal Cord Injury)
- Physiology
- Interruption of Autonomic Pathways, Resulting in Decreased Systemic Vascular Resistance and Altered Vagal Tone: probably the predominant mechanism
- Myocardial Depression: may also play a role
- Acute Blood Loss: may also play a role in some cases
- Physiology
- Brain Herniation (Due to Foramen Magnum Herniation) (see Increased Intracranial Pressure)
- Physiology
- Compression of Brainstem and/or Upper Cervical Spinal Cord
- Physiology
- Chronic Spinal Cord Injury (SCI) (see Acute Spinal Cord Injury)
- Clinical
- Autonomic Dysreflexia (see Autonomic Dysreflexia)
- Clinical
- Guillain-Barre Syndrome (GBS) (see Guillain-Barre Syndrome)
- Epidemiology
- Autonomic Dysfunction is Common in GBS (Occurs in Approximately 66% of Cases)
- Clinical
- Arrhythmias
- Blood Pressure Fluctuations
- Bradycardia/Tachycardia
- Gastrointestinal Dysfunction
- Epidemiology
- Multiple Sclerosis (see Multiple Sclerosis)
- Epidemiology
- Autonomic Dysfunction Can Occur
- Clinical
- Arrhythmias
- Bladder Dysfunction (see xxxx)
- Orthostatic Hypotension (see Orthostatic Hypotension)
- Diaphoresis (see Diaphoresis)
- Gastrointestinal Dysfunction
- Epidemiology
- Neuraxial (Spinal) Anesthesia (see Spinal Anesthesia)
- Physiology
- XXXX
- Physiology
- Transverse Myelitis (see Transverse Myelitis)
- Physiology
- XXXX
- Physiology
- Traumatic Brain Injury (TBI) (see Traumatic Brain Injury)
- Physiology
- XXXX
- Physiology
Drug/Toxin-Associated Hypotension
- Abacavir-Hypersensitivity Reaction (see Abacavir)
- Pharmacology: peripheral vasodilation
- Alcohol Intoxications
- Ethanol (see Ethanol)
- Pharmacology: peripheral vasodilation
- Ethylene Glycol Intoxication (see Ethylene Glycol)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Isopropanol Intoxication (see Isopropanol)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Methanol Intoxication (see Methanol)
- Pharmacology: peripheral vasodilation
- Ethanol (see Ethanol)
- Amiodarone (Cordarone) (see Amiodarone)
- Pharmacology
- Peripheral Vasodilation
- Negative Inotropy Can Also Occur in Patients with Preexisting Left Ventricular Dysfunction with EF <35%)
- Pharmacology
- Atypical Antipsychotics (see Antipsychotic Agents)
- Olanzapine (Zyprexa) (see Olanzapine)
- Quetiapine (Seroquel) (see Quetiapine)
- Risperidone (Risperdal) (see Risperidone)
- Benzodiazepines (see Benzodiazepines)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Capsaicin (see Capsaicin)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Cholinergic Intoxication (see Cholinergic Intoxication)
- Carbamate Intoxication (see Carbamates)
- Organophosphate Intoxication (see Organophosphates)
- Cigua Toxin Poisoning (see Cigua Toxin Poisoning)
- Physiology
- Dysfunction of Calcium and Sodium channels, Resulting in Peripheral Vasodilation
- Physiology
- Cyanide Intoxication (see Cyanide)
- Pharmacology
- Mitochondrial Dysfunction
- Clinical: hypotension occurs late in the course
- Pharmacology
- Cytokine Release Syndrome (see Cytokine Release Syndrome)
- Associated Agents
- Alemtuzumab (Campath, MabCampath, Campath-1H, Lemtrada) (see Alemtuzumab): anti-CD52 monoclonal antibody
- Anti-Thymocyte Globulin (ATG) (see Antithymocyte Globulin)
- Basiliximab (Simulect) (see Basiliximab)
- Bi-Specific Antibodies in Treatment of Leukemia
- Chimeric Antigen Receptor T-Cells (CAR-T) (see Chimeric Antigen Receptor T-Cells)
- Haploidentical Mononuclear Cells in Treatment of Refractory Leukemia
- Lenalidomide (Revlimid) (see Lenalidomide)
- Muromonab-CD3 (Orthoclone OKT3) (see Muromonab-CD3): anti-CD3 monoclonal antibody
- Oxaliplatin (Eloxatin, Oxaliplatin Medac) (see Oxaliplatin)
- Rituximab (Rituxan) (see Rituximab): chimeric monoclonal anti-CD20 antibody
- Tisagenlecleucel (Kymriah) (see Tisagenlecleucel): CAR-T (CD19-directed T-cell medication) therapy
- Pharmacology
- Peripheral Vasodilation
- Associated Agents
- Defibrotide (Defitelio) (see Defibrotide)
- Dexmedetomidine (Precedex) (see Dexmedetomidine)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Differentiation Syndrome (Retinoic Acid Syndrome) (see Tretinoin)
- Epidemiology
- Occurs During Treatment of Acute Promyelocytic Leukemia with Tretinoin (see Acute Promyelocytic Leukemia)
- Pharmacology
- Peripheral Vasodilation
- Epidemiology
- Dobutamine (Dobutrex) (see Dobutamine)
- Pharmacology
- Myocardial β1-Adrenergic Receptor Agonist (Chronotropic/Inotropic Effects) and Vascular β2-Adrenergic/α1-Adrenergic Receptor Agonist (if Vascular β2-Adrenergic Effects exceed α1-Adrenergic Receptor Agonist Effects, Some Peripheral Vasodilation May Occur)
- Pharmacology
- Eltrombopag (Promacta, Revolade)
- Pharmacology
- XXXXX
- Pharmacology
- Endothelin Receptor Antagonists (ERA’s) (see Endothelin Receptor Antagonists)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Envenomations
- Types
- Scorpion Sting (see Scorpion Sting)
- Rattlesnake Bit (see Rattlesnake Bite)
- Widow Spider Bite (see Widow Spider Bite)
- Epidemiology: hypertension is more characteristically seen in widow spider bites, hypotension occurs rarely
- Types
- Estrogen (see Estrogen)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Glyphosate Ingestion (see Glyphosate)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Hemoglobinopathies
- Carboxyhemoglobinemia (see Carboxyhemoglobinemia)
- Pharmacology
- Mitochondrial Dysfunction
- Pharmacology
- Methemoglobinemia (see Methemoglobinemia)
- Physiology
- Peripheral Vasodilation
- Physiology
- Carboxyhemoglobinemia (see Carboxyhemoglobinemia)
- Hexoprenaline (Gynipral) (see Hexoprenaline)
- Pharmacology
- β2-Adrenergic Receptor Agonist
- Pharmacology
- Hydrogen Sulfide Gas Inhalation (see Hydrogen Sulfide Gas)
- Intravenous Immunoglobulin (IVIG) (see Intravenous Immunoglobulin)
- L-Arginine (see L-Arginine)
- Pharmacology
- Nitric Oxide Induction, Resulting in Peripheral Vasodilation
- Pharmacology
- Magnesium Sulfate (see Magnesium Sulfate)
- Epidemiology
- Hypotension May Occur with Rapid Infusion
- Epidemiology
- Metal Intoxications
- N-Acetylcysteine (Mucomyst, Acetadote, Fluimucil, Parvolex) (see N-Acetylcysteine)
- Epidemiology
- Associated with Oral Administration
- Pharmacology
- Peripheral Vasodilation
- Epidemiology
- Nerium Oleander Intoxication (see Nerium Oleander)
- Neuroleptic Malignant Syndrome (NMS) (see Neuroleptic Malignant Syndrome)
- Physiology
- Autonomic Instability
- Physiology
- Nitrites and Nitrates (see Nitrites and Nitrates)
- Pharmacology: nitric oxide induction, resulting in Peripheral Vasodilation
- Ocrelizumab (Ocrevus) (see Ocrelizumab)
- Epidemiology: may occur as a component of infusion reaction
- Opiates (see Opiates)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Papaverine (see Papaverine)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Phenytoin (Dilantin)Fosphenytoin (Cerebyx) (see Fosphenytoin and (see Phenytoin)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Phosphodiesterase Type 5 (PDE5) Inhibitors (see Phosphodiesterase Type 5 Inhibitors)
- Pharmacology: inhibits phosphodiesterase 5/PDE5 (the enzyme which degrades cGMP), resulting in enhanced NO-mediated smooth muscle relaxation and therefore, peripheral vasodilation
- Propofol (Diprivan) (see Propofol)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Prostaglandins with Vasodilatory Properties
- Agents
- Epoprostenol (PGI2, Prostacyclin, Flolan, Veletri) (see Epoprostenol)
- Iloprost (Ilomedin, Ventavis) (see Iloprost)
- Prostaglandin E1 (Alprostadil) (see Prostaglandin E1)
- Pharmacology
- Peripheral Vasodilation
- Agents
- Protamine (see Protamine)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Rasburicase (Elitek) (see Rasburicase)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Ruxolitinib (Jakafi) Withdrawal Syndrome (see Ruxolitinib)
- Epidemiology: occurs 1 day-3 wks after drug withdrawal
- Salicylate Intoxication (see Acetylsalicylic Acid)
- Pharmacology
- Peripheral Vasodilation
- Clinical
- Pseudosepsis with Fever, Tachypnea, Metabolic Acidosis, and Hypotension
- Pharmacology
- Scombroid (see Scombroid)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Serotonin Syndrome (see Serotonin Syndrome)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Sevelamer (Renagel, Renvela) (see Sevelamer)
- Tetrahydrocannabinol (THC) (see Tetrahydrocannabinol)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Tetrodotoxin
- Epidemiology
- Associated with Ingestion of Tetrodotoxin-Contaminated Pufferfish
- Physiology
- Tetrodotoxin Inhibits Sodium Channels on Vascular Smooth Muscle
- Epidemiology
- Theobromine (see Theobromine)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Thrombolytics (see Thrombolytics
- Transfusion-Associated Acute Lung Injury (TRALI) (see Transfusion-Associated Acute Lung Injury)
- Tricyclic Antidepressant Intoxication (see Tricyclic Antidepressants)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Vancomycin-Associated Red Man Syndrome (see Vancomycin)
- Pharmacology
- Peripheral Vasodilation
- Pharmacology
- Vasodilator Antihypertensives
- Agents
- α-Adrenergic Receptor Antagonists (see α-Adrenergic Receptor Antagonists)
- Pharmacology: α2-adrenergic receptor antagonism, resulting peripheral vasodilation
- α-Methyldopa (Aldomet, Aldoril, Dopamet, Dopegyt) (see α-Methyldopa)
- Pharmacology: α2-adrenergic receptor agonist, resulting in peripheral vasodilation
- Angiotensin Converting Enzyme (ACE) Inhibitors (see Angiotensin Converting Enzyme (ACE) Inhibitors)
- Pharmacology: angiotensin converting enzyme inhibition, resulting in peripheral vasodilation
- Angiotensin II Receptor Blockers (ARB) (see Angiotensin II Receptor Blockers)
- Pharmacology: angiotensin II receptor inhibition, resulting in peripheral vasodilation
- β-Adrenergic Receptor Antagonists (β-Blockers) (see β-Adrenergic Receptor Antagonists)
- Pharmacology: β-adrenergic receptor antagonism, resulting in decreased cardiac output and peripheral vasodilation
- Calcium Channel Blockers (see Calcium Channel Blockers)
- Pharmacology: calcium channel antagonism, resulting in peripheral vasodilation (and additionally decreased cardiac output with some of the agents)
- Clonidine (Catapres, Kapvay, Nexiclon) (see Clonidine)
- Pharmacology: α2-adrenergic receptor agonism, resulting in peripheral vasodilation
- Hydralazine (see Hydralazine)
- Pharmacology: peripheral vasodilation
- Minoxidil (see Minoxidil)
- Pharmacology: direct relaxation of arteriolar smooth muscle (possibly mediated by cAMP), resulting in peripheral vasodilation
- α-Adrenergic Receptor Antagonists (see α-Adrenergic Receptor Antagonists)
- Agents
Other
- Cirrhosis/End-Stage Liver Disease (see Cirrhosis)
- Physiology
- Characteristically Produces a High Cardiac Output (CO)/Low Systemic Vascular Resistance (SVR) State
- Physiology
- Hepatic Veno-Occlusive Disease (see Hepatic Veno-Occlusive Disease)
- Hypercapnia (see Hypercapnia and Respiratory Failure)
- Physiology
- Hypercapnia-Induced Venodilation
- Physiology
- Hypoxemia (see Hypoxemia and Respiratory Failure)
- Physiology
- Hypoxia-Induced Systemic Vasodilation (Which Attempts to Maintain Tissue Perfusion with Oxygen Delivery)
- In Contrast, in the Pulmonary Circulation, Hypoxia Results in Hypoxic Pulmonary Vasoconstriction
- Hypoxia-Induced Systemic Vasodilation (Which Attempts to Maintain Tissue Perfusion with Oxygen Delivery)
- Physiology
- Pregnancy (see Pregnancy)
- Physiology: pregnancy increases plasma volume, increases cardiac output, increases stroke volume, increases heart rate, decreases blood pressure, and decreases SVR
- Purpura Fulminans (see Purpura Fulminans)
- Systemic Arteriovenous Fistula (see Systemic Arteriovenous Fistula)
- Types
- Femoral Arteriovenous Fistula: most common type of acquired arteriovenous fistula (due to the frequency of using the femoral site for percutaneous arterial or venous access)
- Hemodialysis Arteriovenous Fistula (see Hemodialysis Arteriovenous Fistula)
- Clinical: high output heart failure may occur
- Types
- Systemic Mastocytosis (see Systemic Mastocytosis)
- Physiology
- Peripheral Vasodilation
- Physiology
- Vasoplegic Syndrome (Post-Cardiac Surgery Vasodilation) (see Vasoplegic Syndrome)
- Physiology
- Peripheral Vasodilation Following Cardiac Surgery
- Physiology
- Vasovagal Syncope (see Vasovagal Syncope)
- Physiology
- Peripheral Vasodilation
- Physiology
Hemorrhagic Shock (see Hemorrhagic Shock)
Gastrointestinal Hemorrhage (see Gastrointestinal Hemorrhage)
- Lower Gastrointestinal Hemorrhage (see Gastrointestinal Hemorrhage)
- Upper Gastrointestinal Hemorrhage (see Gastrointestinal Hemorrhage)
Hemoperitoneum (see Hemoperitoneum)
- Various Etiologies
Intramuscular Hemorrhage (Into Thigh)
- Various Etiologies
Intraoperative/Postoperative Hemorrhage
- Various Etiologies
Retroperitoneal Hemorrhage (see Retroperitoneal Hemorrhage)
- Ruptured Abdominal Aortic Aneurysm (AAA) (see Abdominal Aortic Aneurysm)
- Other Etiologies
Severe Hemolysis (see Hemolytic Anemia)
- Sickle Cell Crisis (see Sickle Cell Disease)
Trauma with External Hemorrhage
- Motor Vehicle Accident (MVA)
- Traumatic Fall/Assault
Uterine/Vaginal Hemorrhage
- Postpartum Hemorrhage
- Primary Postpartum Hemorrhage (see Postpartum Hemorrhage-Primary)
- Secondary (Late) Postpartum Hemorrhage (see Postpartum Hemorrhage-Secondary)
- Uterine Tumor
- Vaginal Laceration
Other
- Ruptured Left Ventricular Aneurysm (see Left Ventricular Aneurysm)
Hypovolemic Shock (see Hypovolemic Shock)
Dermal Fluid Loss
- Altered Mental Status with Inadequate Fluid Intake
- Intoxication
- Burns (see Burns)
- Diaphoresis (see Diaphoresis)
- Heat Stroke/Environmental Exposure (see Heat Stroke)
Gastrointestinal Fluid Loss
- Diarrhea (see Diarrhea)
- Early Dumping Syndrome (After Gastric Bypass) (see Dumping Syndrome and Gastric Bypass)
- Physiology: hyperosmolality of food causes rapid fluid shift from the plasma into the bowel
- External Drainage
- Vomiting (see Nausea and Vomiting)
Renal Fluid Loss
- Excessive Diuresis
- Hypoaldosteronism (see Hypoaldosteronism)
- Epidemiology: although aldosterone normally acts to increase sodium retention, hypoaldosteronism is not usually associated with significant sodium wasting (except in young children)
- This is due to the compensatory action of other sodium-retaining stimuli (such as angiotensin II and norepinephrine)
- Epidemiology: although aldosterone normally acts to increase sodium retention, hypoaldosteronism is not usually associated with significant sodium wasting (except in young children)
- Pheochromocytoma (see Pheochromocytoma)
- Epidemiology: occurs in some cases
- Clinical Patterns
- Episodic Hypotension: in rare cases where the tumor secretes only epinephrine
- Pattern of Rapid Cyclic Fluctuation Between Hypertension and Hypotension (Cycling Every 7-15 min): unclear mechanism
- Orthostatic Hypotension: due predominantly to decreased plasma volume
- Salt-Wasting Nephropathy
Third-Space Fluid Loss
- Acute Pancreatitis (see Acute Pancreatitis)
- Cirhosis (see Cirrhosis)
- Crush Injury
- Intestinal Obstruction
- Colonic Obstruction (see Colonic Obstruction)
- Small Bowel Obstruction (SBO) (see Small Bowel Obstruction)
- Post-Operative Intraabdominal Fluid Loss
- Trauma
Diagnostic
Arterial Line (see Arterial Line)
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Bedside Ultrasound
Clinical Efficacy
- SHoC-ED International Randomized, Controlled Trial of Bedside Ultrasound in Undifferentiated Hypotension in the Emergency Department (Ann Emerg Med, 2018) [MEDLINE]: n= 273
- The Most Common Diagnosis in >50% of the Patients was Occult Sepsis
- Bedside (Point-of-Care) Ultrasound Did Not Impact the Mortality Rate, ICU or Total Length of Stay, Rate of CT Scanning, Inotrope Use, or Intravenous Fluid Administration in Undifferentiated Hypotension
Echocardiogram (see Echocardiogram)
- xxxx
Clinical Manifestations
Cardiovascular Manifestations
- Hypotension (see Hypotension)
- Sinus Tachycardia (see Sinus Tachycardia)
Neurologic Manifestations
- Altered Mental Status
- Delirium (see Delirium)
- Obtundation/Coma (see Obtundation-Coma)
- Fatigue (see Fatigue)
- Increased Intracranial Pressure (see Increased Intracranial Pressure)
- Physiology: hypotension causes cerebral vasodilation
- Clinical: potentiation of neurologic injury in traumatic brain injury (TBI), etc
Renal Manifestations
- Acute Kidney Injury (AKI) (see Acute Kidney Injury)
- Physiology
- Acute Tubular Necrosis (ATN)
- Impaired Renal Perfusion
- Physiology
Treatment
Vasopressors
- xxxx
References
- Does Point-of-Care Ultrasonography Improve Clinical Outcomes in Emergency Department Patients With Undifferentiated Hypotension? An International Randomized Controlled Trial From the SHoC-ED Investigators. Ann Emerg Med. 2018 Oct;72(4):478-489. doi: 10.1016/j.annemergmed.2018.04.002 [MEDLINE]