Hypotension 
Etiology 
Arrhythmia/Conduction Disturbance 
Bradyarrhythmia 
Tachyarrythmia 
 
Primary Cardiomyopathies (Predominantly Involving the Heart) 
Genetic 
Arrhythmogenic Right Ventricular Cardiomyopathy (Arrhythmogenic Right Ventricular Dysplasia) (see Arrhythmogenic Right Ventricular Cardiomyopathy ) 
Conduction System Disease
 
Glycogen Storage Diseases
 
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 ) 
 
 
Secondary Cardiomyopathies 
Cardiofacial 
Lentiginosis 
Noonan Syndrome 
 
Endocrine/Metabolic 
Endomyocardial 
Hematologic Disease 
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 ) 
 
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)
 
 
Neoplasm 
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 
Carnitine Deficiency (see Carnitine ) 
Keshan’s Disease 
Kwashiorkor 
Niacin Deficiency (Pellagra) (see Niacin ) 
Selenium Deficiency (see Selenium ) 
Thiamine Deficiency (Beriberi) (see Thiamine ) 
Vitamin C Deficiency (Scurvy) (see Vitamin C ) 
 
Rheumatologic 
Storage (Accumulation of Abnormal Substances Intracellularly Within Myocytes) 
Traumatic 
Drug/Toxin 
Other 
 
 
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 
 
 
Hypertrophic Obstructive Cardiomyopathy (HOCM)  (see Hypertrophic Cardiomyopathy )Malignant Hypertension  (see Hypertension )
Physiology 
Left Ventricular Pressure Overload 
 
 
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 
 
 
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 
 
 
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 
 
 
 
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 )
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 
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 
 
 
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 
 
 
 
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 
 
 
 
Hemothorax  (see Pleural Effusion-Hemothorax )
Physiology
Increased Intrathoracic Pressure, Resulting in Impaired Right-Sided Venous Return 
 
 
 
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 
 
 
 
Positive-Pressure Ventilation with High Airway Pressures  (see Acute Respiratory Distress Syndrome )
Physiology
Increased Intrathoracic Pressure, Resulting in Impaired Right-Sided Venous Return 
 
 
 
Tension Pneumothorax  (see Pneumothorax 
Physiology
Increased Intrathoracic Pressure, Resulting in Impaired Right-Sided Venous Return 
 
 
 
 
 
Pulmonary Vascular 
 
Distributive Shock (Vasodilatory Shock) 
Anaphylaxis/Anaphylactic Shock 
Anaphylaxis  (see Anaphylaxis )
Physiology 
Peripheral Vasodilation (Due to Histamine and Other Vasoactive Substances) 
 
 
 
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 
 
 
Toxic Shock Syndrome (TSS) 
 
Systemic Inflammatory Response Syndrome (SIRS) (see Sepsis ) 
Endocrine/Metabolic/Nutritional Deficiency-Associated Hypotension 
Acidemia 
Adrenal Insufficiency  (see Adrenal Insufficiency )
Hyperthyroidism  (see Hyperthyroidism )
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 
 
 
Hypothyroidism/Myxedema  (see Hypothyroidism )
Pheochromocytoma  (see Pheochromocytoma )
Epidemiology 
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 
 
 
Thiamine Deficiency (Beriberi)  (see Thiamine )
 
Hematologic Disease-Associated Hypotension 
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 
 
 
Brain Herniation (Due to Foramen Magnum Herniation)  (see Increased Intracranial Pressure )
Physiology 
Compression of Brainstem and/or Upper Cervical Spinal Cord 
 
 
Chronic Spinal Cord Injury (SCI)  (see Acute Spinal Cord Injury )
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 
 
 
Multiple Sclerosis  (see Multiple Sclerosis )
Epidemiology 
Autonomic Dysfunction Can Occur 
 
Clinical 
 
Neuraxial (Spinal) Anesthesia  (see Spinal Anesthesia )
Transverse Myelitis  (see Transverse Myelitis )
Traumatic Brain Injury (TBI)  (see Traumatic Brain Injury )
 
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 )
Isopropanol Intoxication  (see Isopropanol )
Methanol Intoxication  (see Methanol )
Pharmacology: peripheral vasodilation 
 
 
Amiodarone (Cordarone)  (see Amiodarone )
Pharmacology 
Peripheral Vasodilation 
Negative Inotropy Can Also Occur in Patients with Preexisting Left Ventricular Dysfunction with EF <35%) 
 
 
Atypical Antipsychotics  (see Antipsychotic Agents )
Benzodiazepines  (see Benzodiazepines )
Capsaicin  (see Capsaicin )
Cholinergic Intoxication  (see Cholinergic Intoxication )
Cigua Toxin Poisoning  (see Cigua Toxin Poisoning )
Physiology 
Dysfunction of Calcium and Sodium channels, Resulting in Peripheral Vasodilation 
 
 
Cyanide Intoxication  (see Cyanide )
Pharmacology 
Mitochondrial Dysfunction 
 
Clinical : hypotension occurs late in the course 
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 
 
Defibrotide (Defitelio)  (see Defibrotide )Dexmedetomidine (Precedex)  (see Dexmedetomidine )
Differentiation Syndrome (Retinoic Acid Syndrome)  (see Tretinoin )
Epidemiology 
Pharmacology 
 
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) 
 
 
Eltrombopag (Promacta, Revolade) 
Endothelin Receptor Antagonists (ERA’s)  (see Endothelin Receptor Antagonists )
Envenomations 
Estrogen  (see Estrogen )
Glyphosate Ingestion  (see Glyphosate )
Hemoglobinopathies 
Hexoprenaline (Gynipral)  (see Hexoprenaline )
Pharmacology 
β2-Adrenergic Receptor Agonist 
 
 
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 
 
 
Magnesium Sulfate  (see Magnesium Sulfate )
Epidemiology 
Hypotension May Occur with Rapid Infusion 
 
 
Metal Intoxications 
N-Acetylcysteine (Mucomyst, Acetadote, Fluimucil, Parvolex)  (see N-Acetylcysteine )
Epidemiology 
Associated with Oral Administration 
 
Pharmacology 
 
Nerium Oleander  IntoxicationNerium Oleander )Neuroleptic Malignant Syndrome (NMS)  (see Neuroleptic Malignant Syndrome )
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 )
Papaverine  (see Papaverine )
Phenytoin (Dilantin)Fosphenytoin (Cerebyx)  (see Fosphenytoin  and (see Phenytoin )
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 )
Prostaglandins with Vasodilatory Properties 
Protamine  (see Protamine )
Rasburicase (Elitek)  (see Rasburicase )
Ruxolitinib (Jakafi) Withdrawal Syndrome  (see Ruxolitinib )
Epidemiology : occurs 1 day-3 wks after drug withdrawal 
Salicylate Intoxication  (see Acetylsalicylic Acid )
Pharmacology 
Clinical 
Pseudosepsis with Fever, Tachypnea, Metabolic Acidosis, and Hypotension 
 
 
Scombroid  (see Scombroid )
Serotonin Syndrome  (see Serotonin Syndrome )
Sevelamer (Renagel, Renvela)  (see Sevelamer )Tetrahydrocannabinol (THC)  (see Tetrahydrocannabinol )
Tetrodotoxin 
Epidemiology 
Associated with Ingestion of Tetrodotoxin-Contaminated Pufferfish 
 
Physiology 
Tetrodotoxin Inhibits Sodium Channels on Vascular Smooth Muscle 
 
 
Theobromine  (see Theobromine )
Thrombolytics  (see Thrombolytics Transfusion-Associated Acute Lung Injury (TRALI)  (see Transfusion-Associated Acute Lung Injury )Tricyclic Antidepressant Intoxication  (see Tricyclic Antidepressants )
Vancomycin-Associated Red Man Syndrome  (see Vancomycin )
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 
 
 
 
 
 
Other 
Cirrhosis/End-Stage Liver Disease  (see Cirrhosis )
Physiology 
Characteristically Produces a High Cardiac Output (CO)/Low Systemic Vascular Resistance (SVR) State 
 
 
Hepatic Veno-Occlusive Disease  (see Hepatic Veno-Occlusive Disease )Hypercapnia  (see Hypercapnia  and Respiratory Failure )
Physiology 
Hypercapnia-Induced Venodilation 
 
 
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 
 
 
 
 
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 
Systemic Mastocytosis  (see Systemic Mastocytosis )
Vasoplegic Syndrome (Post-Cardiac Surgery Vasodilation)  (see Vasoplegic Syndrome )
Physiology 
Peripheral Vasodilation Following Cardiac Surgery 
 
 
Vasovagal Syncope  (see Vasovagal Syncope )
 
 
Intramuscular Hemorrhage (Into Thigh) 
Intraoperative/Postoperative Hemorrhage 
Trauma with External Hemorrhage 
Motor Vehicle Accident (MVA) Traumatic Fall/Assault  
Uterine/Vaginal Hemorrhage 
Postpartum Hemorrhage 
Uterine Tumor Vaginal Laceration  
Other 
 
Dermal Fluid Loss 
Altered Mental Status with Inadequate Fluid Intake 
Burns  (see Burns )Diaphoresis  (see Diaphoresis )Heat Stroke/Environmental Exposure  (see Heat Stroke ) 
Gastrointestinal Fluid Loss 
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) 
 
 
Pheochromocytoma  (see Pheochromocytoma )
Epidemiology : occurs in some casesClinical 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 
Post-Operative Intraabdominal Fluid Loss Trauma  
 
Diagnostic 
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  
 
Clinical Manifestations 
Cardiovascular Manifestations 
Neurologic Manifestations 
Altered Mental Status 
Fatigue  (see Fatigue )Increased Intracranial Pressure  (see Increased Intracranial Pressure )
Physiology : hypotension causes cerebral vasodilationClinical : 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 
 
 
 
Treatment 
Vasopressors 
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 ] 
 
 
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