Hemodynamics


Blood Pressure

Blood Pressure Measurement Technique

  • Sphygmomanometer (see Sphygmomanometer)
    • Allows Nonivasive Measurement of Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP)
    • Noninvasive Cuff Measurement of Blood Pressure (Especially Automated Cuff Measurement) is Less Accurate in Shock States (JAMA, 1967) [MEDLINE]
  • Arterial Line (see Arterial Line)
    • Allows Invasive Measurement of Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP)
    • Arterial Line Placement with Invasive Blood Pressure Measurement is Generally Recommended in the Setting of Shock (Especially When Vasopressors are Required)

Equation for the Mean Arterial Pressure (MAP)

  • MAP = [(2 x DBP) + (SBP)]/3
    • Twice as Much of the Cardiac Cycle is Spent in Diastole, Relative to Systole
    • Terms
      • MAP: mean arterial blood pressure (in mm Hg)
      • SBP: systolic blood pressure (in mm Hg)
      • DBP: diastolic blood pressure (in mm Hg)
    • Normal MAP: 85-95 mm Hg


Cardiac Output (CO)

Cardiac Output Measurement Technique

Thermodilution Cardiac Output (Utilizing a Swan-Ganz Catheter) (see Swan-Ganz Catheter)

  • Thermodilution Method Allows Measurement of Cardiac Output Using the Injection of Cold Saline through a Port on the Swan-Ganz Catheter, Using a Temperature-Sensitive Thermistor on the Catheter to Measure the Rate of Clearance of the Cold Saline
    • Utilizing Principles Developed by Fick in the Late 19th Century, the Rate of Clearance of Cold Saline is Proportional to the Blood Flow Rate (i.e. Cardiac Output)
    • The Area Under the Thermodilution Curve is Inversely Related to the Cardiac Output (i.e. High Cardiac Output Results in Rapid Clearance of the Cold Saline, Resulting in a Small Area Under the Curve)
  • Variability in Serial Thermodilution Cardiac Output Measurements
    • Variability in Cardiac Output Values Obtained by Thermodilution is Approximately 10%
      • Therefore, Changes in Cardiac Output Should Generally Be on the Order of 15% to Be Regared as Valid
  • Etiology of Falsely Decreased Cardiac Output
    • Tricuspid Regurgitation (TR) (see Tricuspid Regurgitation: local “recirculation” of injectate mimics slow injectate clearance
    • Pulmonic Regurgitation (see Pulmonic Regurgitation): local “recirculation” of injectate mimics slow injectate clearance
    • Erroneously High Cold Saline Injectate Volume
  • Etiology of Falsely Increased Cardiac Output
    • Intracardiac Shunt (in Either Direction) (see Intracardiac and Extracardiac Shunt): alters curve and makes cardiac output calculation less accurate
    • Low Cardiac Output State: injectate can disperse into the surrounding tissue, mimicking rapid injectate clearance
    • Erroneously Low Cold Saline Injectate Volume
  • Early Recirculation on Thermodilution Curve
    • Suggests Presence of Left-to-Right Intracardiac Shunt
  • Continuous Cardiac Output Measurement
    • Swan-Ganz Catheters with the Capability to Measure Cardiac Output “continuously” (Actually Averages the Cardiac Output Over a Few Minute Window) are Commercially Available

Fick Cardiac Output

  • Fick Cardiac Output = Oxygen Consumption/(10 x Arterial-Venous Oxygen Difference)
  • Determination of Oxygen Consumption
    • Oxygen Consumption (Estimated) Can Be Obtained from a Nomogram Which Utilizes Age, Sex, Height, and Weight
    • Oxygen Consumption Can Also Be Determined Using Breath Analysis

FloTrac (see FloTrac)

  • Noninvasive Cardiac Output Measurement Device
  • Requires Arterial Line Placement and Vigileo Monitor (see Arterial Line)

Cardiac Output Equation

  • CO = SV x HR
  • CO = [(LV-EF x LV-EDV) – MR] x HR
    • Terms
      • CO: cardiac output
      • SV: stroke volume = (LV-EF x LV-EDV) – MR
      • HR: heart rate
      • LV-EF: left ventricular ejection fraction
      • LV-EDV: left ventricular end-diastolic volume
      • MR: mitral regurgitation

Etiology of Decreased Cardiac Output

Cardiogenic Shock (Cardiac Pump Failure Due to a Cardiac Etiology) (see Cardiogenic Shock)

Arrhythmia/Conduction Disturbance
Cardiomyopathy (see Congestive Heart Failure)
    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)
      • 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
    • 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

    Etiology of Increased Cardiac Output (J Am Coll Cardiol, 2016) [MEDLINE])

    General Comments

    • Many of the Following Conditions are Classified as Etiologies of “High Output Heart Failure”
      • However, this Term is a Misnomer, Since the Heart is Generally Normal (Capable of Generating a High Cardiac Output) and the Underlying Pathophysiology is Decreased Systemic Vascular Resistance, Resulting in Activation of Neurohormones Which Increase Renal Salt and Water Retention (and May Result in Hypotension)
      • Treatment with Vasodilators (Typically Used in Congestive Heart Failure) May Exacerbate the Heart Failure in These Conditions

    Conditions with Predominant Peripheral Vascular Effects

    • Carcinoid Syndrome (see Carcinoid Syndrome)
      • Physiology
        • Peripheral Vasodilation with Decreased Systemic Vascular Resistance
      • Clinical
        • High Cardiac Output/Low Systemic Vascular Resistance State Has Been Reported in Some Cases (Ann Intern Med, 1994) [MEDLINE] (Neth J Med, 2002) [MEDLINE]
          • However, Heart Failure with Right Heart Valvular Fibrosis is a More Common Cardiac Presentation
    • Cirrhosis/Liver Disease (see Cirrhosis)
      • Physiology
        • Progressive Systemic Vasodilation (Especially Splanchnic) with Development of Intrahepatic/Mesenteric Arteriovenous Shunts
        • Intrapulmonary Arteriovenous Shunts (i.e. Hepatopulmonary Syndrome) May Also Occur (Echocardiography, 2006) [MEDLINE] (see Hepatopulmonary Syndrome)
      • Clinical
        • Characteristically Produces a High Cardiac Output/Low Systemic Vascular Resistance State
        • High Output Heart Failure May Occur
        • Of All of the High Output Heart Failure Conditions, Cirrhosis Generally Produces the Lowest Arterial-Venous Oxygen Difference and the Lowest Systemic Vascular Resistance
    • Erythroderma (of Any Etiology) (see Erythroderma)
      • Etiology
        • Drug Hypersensitivity Reaction
        • Psoriasis (see Psoriasis)
      • Physiology
        • Significant Cutaneous Vasodilation and Increased Blood Flow to the Skin, Resulting in Shunting of Blood Flow Through the Skin
    • Morbid Obesity (see Obesity)
      • Physiology
        • Peripheral Vasodilation with Decreased Systemic Vascular Resistance (of Unclear Etiology)
        • Leptin-Induced Expansion of Plasma Volume and Eccentric Ventricular Dilation/Hypertrophy (Circulation, 2018) [MEDLINE]
        • Obesity-Associated Hypertension (with Pressure Overload) Likely Exacerbates the Effect of Obesity on Cardiac Output (Physiol Rep, 2015) [MEDLINE]
      • Clinical
        • High Cardiac Output (Although Cardiac Output is Normal When Adjusted for Body Weight)
    • Systemic Arteriovenous Fistula (AVF) (see Systemic Arteriovenous Fistula)
      • Etiology
        • Aortocaval Fistula (Due to Spontaneous Rupture of Aortic Aneurysm)
        • Congenital Arteriovenous Fistula
        • Highly Vascular Condition/Tumor
        • Iatrogenic
          • Femoral/Radial/Ulnar Arteriovenous Fistula (Due to Arterial Access for Cardiac Catheterization for Coronary Angiogram)
          • Iliac Arteriovenous Fistula (Due to Spinal/Abdominal Surgery)
          • Renal Arteriovenous Fistula (Due to Renal Biopsy)
          • Surgically-Constructed Arteriovenous Access for Hemodialysis
          • Transjugular Intrahepatic Portosystemic Shunt (TIPS) (see Transjugular Intrahepatic Portosystemic Shunt)
        • Multiple Myeloma (see Multiple Myeloma): due to multiple minute arteriovenous fistulas in bony lesions
        • Paget Disease of the Bone (Osteitis Deformans) (see Paget Disease of Bone): due to multiple minute arteriovenous fistulas in bony lesions
        • Polyostotic Fibrous Dysplasia (McCune-Albright Syndrome): due to multiple minute arteriovenous fistulas in bony lesions
        • Trauma
          • Aortocaval Fistula
          • Bullet/Knife Wound (Particularly in the Thigh)
      • Physiology
        • High Pressure Arterial Blood is Shunted into a Low Pressure Vein, Shunting Past the Tissue Capillary Bed (and Decreasing the Systemic Vascular Resistance)
          • Subsequently, there is a Compensatory Increase in Stroke Volume, Cardiac Output, and Total Plasma Volume to Maintain Capillary Perfusion
      • Clinical

    Conditions with Predominant Metabolic Effects

    • Hyperthyroidism (see Hyperthyroidism)
      • Physiology
        • Enhanced Sympathoadrenal Activation
        • Direct Myocardial Chronotropic and Inotropic Effects
        • Hyperthyroidism-Associated β-Adrenergic Stimulation Has Been Proposed to Have a Cardiotoxic Effect (Heart, 2007) [MEDLINE]
      • Clinical
        • Widened Pulse Pressure (see Widened Pulse Pressure)
        • High Cardiac Output/Low Systemic Vascular Resistance State May Occur (with High Output Heart Failure) (NEJM, 2001) [MEDLINE]
          • Sympatholytic Agents (β-Blockers) Can Partially Decrease Heart Rate and Cardiac Output, as Well as Partially Improve Pulse Pressure
        • Hyperthyroidism-Associated Hyperdynamic Right Ventricular Function (Which is Reversible with Treatment) Has Also Been Reported (Heart Lung Circ, 2017) [MEDLINE]
        • Hyperthyroidism-Associated Decreased Cardiac Output May Alternately Occur (Due to Tachycardia-Mediated Cardiomyopathy or Associated Cardiac Disease) (Heart, 2007) [MEDLINE]
        • Hyperthyroidism-Associated Reversible Right Ventricular Failure with Pulmonary Hypertension Has Also Been Reported (Am J Med Sci, 2018) [MEDLINE]
    • Myeloproliferative Disorders with Extramedullary Hematopoiesis
      • Etiology
      • Physiology
        • Increased Metabolic State with Increased Oxygen Consumption and Decreased Systemic Vascular Resistance

    Conditions with Myocardial and Peripheral Vascular Effects

    • Acromegaly (see Acromegaly)
      • Epidemiology
        • Heart Failure May Be Present in Newly-Diagnosed Acromegaly
      • Physiology
        • Growth Hormone is Involved in the Maintenance of Normal Cardiac Function
    • Anagrelide (Agrylin, Xagrid) (see Anagrelide)
      • Epidemiology
      • Pharmacology
        • Phosphodiesterase III Inhibition, Resulting in Positive Inotropic/Chronotropic Effects and Vasodilation
    • 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)
    • Milrinone (see Milrinone)
      • Pharmacology
        • Phosphodiesterase Type 3 Inhibitor (Which Inhibits cAMP Degradation), Resulting in Increased Myocardial Contractility and Vasodilation
    • Mitochondrial Disease
      • Physiology
        • Altered Oxidative Metabolism
      • Clinical
        • Cardiomyopathy
        • Decreased Systemic Vascular Resistance (SVR)
        • Lactic Acidosis (see Lactic Acidosis)
    • Sepsis (see Sepsis)
      • Physiology
        • Due to Inflammatory Response (Involving TNF-α, IL-1β, IL-6, etc)
      • Clinical
        • Characteristically Produces a High Cardiac Output/Low Systemic Vascular Resistance State (Although Sepsis-Induced Myocardial Dysfunction May Alternately Occur)
        • High Output Heart Failure May Occur
    • Thiamine (Vitamin B1) Deficiency (Beriberi) (see Thiamine)
      • Physiology
        • Vasodilation May Occur Due to Direct Depression of Vasomotor Function (Am J Med, 1966) [MEDLINE]
        • Thiamine Deficiency Impairs Lactate and Pyruvate Utilization by the Myocardium (These Substrates are Important for Oxidation and Energy Production in the Myocardium)
        • Thiamine Deficiency Impairs Hexose Monophosphate Shunt Function, Impairing Tissue Oxygenation
      • Clinical
        • Initially Presents with High Cardiac Output/Low Systemic Vascular Resistance State with Increased Blood Volume (Am J Med, 1966) [MEDLINE]
          • High Output Heart Failure May Occur
        • Later, Low Cardiac Output State is Observed (J Am Coll Cardiol, 1989) [MEDLINE]

    Other

    • Anemia (Chronic, Severe) (see Anemia)
      • Epidemiology
        • May Occur in Patients with Beta-Thalassemia Intermedia (see Thalassemias)
      • Physiology
        • Endothelial Dysfunction, Resulting in Peripheral Vasodilation
        • Decreased Serum Viscosity, Resulting in Decreased Left Ventricular Afterload
        • Loss of Hemoglobin is Partly Compensated for by an Increase in Cardiac Output and Widening of the Arteriovenous O2 Difference
          • Severe Anemia Can Result in Left Ventricular Volume Overload and Increased Stroke Volume
      • Clinical
        • Heart Failure Generally Occurs in the Absence of Underlying Heart Disease Only with Severe Anemia (Hemoglobin <5 g/dL)
    • Anxiety or Physical/Emotional Stress (see Anxiety)
      • Physiology
        • Stress Induces Catecholamine Release, Resulting in Increased Cardiac Output and Variable effects on Systemic Vascular Resistance
    • Chronic Pulmonary Disease
      • Epidemiology
        • Chronic Pulmonary Disease Associated with Hypoxemia and/or Hypercapnia is Associated with High Output Heart Failure
      • Physiology
        • Decreased Systemic Vascular Resistance (SVR)
        • Impaired Renal Blood Flow
        • Salt and Water Retention
    • Exercise
      • Physiology
        • During Exercise, Cardiac Output Increases and Systemic Vascular Resistance Decreases
    • Fever (see Fever)
      • Physiology
        • Fever Increases Metabolic Demand and Produces Vasodilation (Especially in the Skin)
    • Hot Climate
      • Physiology
        • Hot (and Especially Humid) Environment Increases Cardiac Output (Similar to Fever)
    • Pregnancy (see Pregnancy)
      • Physiology
        • Decreased Systemic Vascular Resistance (SVR)
        • Increased Blood Volume
        • Increased Maternal Heart Rate (by 15-20 bpm)
        • Increased Metabolic Demand
        • Increased Resting Cardiac Output (to 30-50% Above Baseline)
        • Placental Blood Flow (Which May Function an Arteriovenous Shunt)


    Systemic Vascular Resistance (SVR)

    Calculation of Systemic Vascular Resistance (SVR) Using Pressures Measured from Swan-Ganz Catheter (see Swan-Ganz Catheter)

    • Calculation Technique
      • Systemic Vascular Resistance (SVR) is Calculated from the Mean Arterial Pressure (MAP), Central Venous Pressure (CVP), and Cardiac Output (CO)
        • Unlike, Systemic Vascular Resistance, All Three of These Latter Parameters are Measured
    • Equation: SVR = [(MAP-CVP)/CO] x 80
      • Normal SVR Values (using dynes-sec/cm5): 770-1500 dynes-sec/cm5
      • Note: SVR normal values can alternatively be expressed as 9–20 Woods units (9-20 mm Hg-min/L) -> to convert from Woods units to dynes-sec/cm5, multiply by 80

        Etiology of Decreased Systemic Vascular Resistance (Distributive 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)

        • Acute Pancreatitis (see Acute Pancreatitis)
          • Physiology
            • Third-Spacing of Fluids (with Decreased Intravascular Volume) and Peripheral Vasodilation
        • Air Embolism (see Air Embolism)
          • Physiology
            • Arterial Air Embolism
              • Air Bubbles Occlude the Arterial Microcirculation, Resulting in Ischemia-Induced Endothelial Damage and Release of Inflammatory Mediators, Culminating in End-Organ Injury
            • Venous Air Embolism
              • Air Bubbles in the Pulmonary Microcirculation Result in Local Endothelial Damage, Culminating in Bronchospasm/Acute Lung Injury
        • 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/Nutritional Deficiency-Associated Hypotension

            • Adrenal Insufficiency (see Adrenal Insufficiency)
              • Physiology
                • Peripheral Vasodilation
            • Hyperthyroidism (see Hyperthyroidism)
              • Physiology
                • XXXX
            • 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)
              • Physiology
                • Peripheral Vasodilation
            • 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
            • Thiamine Deficiency (Beriberi) (see Thiamine)
              • Physiology
                • Peripheral Vasodilation

                Hematologic Disease-Associated Hypotension

                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
                • 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)
                  • Physiology
                    • XXXX
                • Transverse Myelitis (see Transverse Myelitis)
                  • Physiology
                    • XXXX
                • Traumatic Brain Injury (TBI) (see Traumatic Brain Injury)
                  • Physiology
                    • XXXX

                  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
                    • Isopropanol Intoxication (see Isopropanol)
                      • Pharmacology
                        • Peripheral Vasodilation
                    • 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)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Capsaicin (see Capsaicin)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • 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
                      • Peripheral Vasodilation
                  • Defibrotide (Defitelio) (see Defibrotide)
                  • Dexmedetomidine (Precedex) (see Dexmedetomidine)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Differentiation Syndrome (Retinoic Acid Syndrome) (see Tretinoin)
                    • Epidemiology
                    • Pharmacology
                      • Peripheral Vasodilation
                  • 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)
                    • Pharmacology
                      • XXXXX
                  • Endothelin Receptor Antagonists (ERA’s) (see Endothelin Receptor Antagonists)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Envenomations
                  • Estrogen (see Estrogen)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Glyphosate Ingestion (see Glyphosate)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • 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
                    • Agents
                    • Pharmacology
                      • Peripheral Vasodilation
                  • N-Acetylcysteine (Mucomyst, Acetadote, Fluimucil, Parvolex) (see N-Acetylcysteine)
                    • Epidemiology
                      • Associated with Oral Administration
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Nerium Oleander Intoxication (see Nerium Oleander)
                  • Neuroleptic Malignant Syndrome (NMS) (see Neuroleptic Malignant Syndrome)
                    • Physiology
                      • Autonomic Instability
                  • Nitrites and Nitrates (see Nitrites and Nitrates)
                    • Pharmacology
                      • Nitric Oxide Induction, Resulting in Peripheral Vasodilation
                  • Ocrelizumab (Ocrevus) (see Ocrelizumab)
                    • Epidemiology
                      • Hypotension May Occur as a Component of Infusion Reaction
                  • Opiates (see Opiates)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Papaverine (see Papaverine)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Phenytoin (Dilantin)Fosphenytoin (Cerebyx) (see Fosphenytoin and (see Phenytoin)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Phosphodiesterase Type 5 (PDE5) Inhibitors (see Phosphodiesterase Type 5 Inhibitors)
                    • Pharmacology
                      • Inhibition of 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
                  • Prostaglandins with Vasodilatory Properties
                    • Agents
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Protamine (see Protamine)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Rasburicase (Elitek) (see Rasburicase)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Ruxolitinib (Jakafi) Withdrawal Syndrome (see Ruxolitinib)
                    • Epidemiology
                      • Ruxolitinib Withdrawal Syndrome 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
                  • Scombroid (see Scombroid)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Serotonin Syndrome (see Serotonin Syndrome)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Sevelamer (Renagel, Renvela) (see Sevelamer)
                  • Tetrahydrocannabinol (THC) (see Tetrahydrocannabinol)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Tetrodotoxin
                    • Epidemiology
                      • Associated with Ingestion of Tetrodotoxin-Contaminated Pufferfish
                    • Physiology
                      • Tetrodotoxin Inhibits Sodium Channels on Vascular Smooth Muscle
                  • Theobromine (see Theobromine)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Thrombolytics (see Thrombolytics
                  • Transfusion-Associated Acute Lung Injury (TRALI) (see Transfusion-Associated Acute Lung Injury)
                  • Tricyclic Antidepressant Intoxication (see Tricyclic Antidepressants)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • Vancomycin-Associated Red Man Syndrome (see Vancomycin)
                    • Pharmacology
                      • Peripheral Vasodilation
                  • 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

                  • Acidemia (see Metabolic Acidosis-Elevated Anion Gap and Metabolic Acidosis-Normal Anion Gap)
                    • Physiology
                      • Acidemia-Associated Arterial Vasodilation, Venoconstriction, and Blunted Response to Catecholamines
                  • Cirrhosis/End-Stage Liver Disease (see Cirrhosis)
                    • Physiology
                      • Liver Disease Characteristically Produces a High Cardiac Output (CO)/Low Systemic Vascular Resistance (SVR) State
                  • Hepatic Sinusoidal Obstruction Syndrome (Hepatic Veno-Occlusive Disease (see Hepatic Sinusoidal Obstruction Syndrome)
                    • Epidemiology
                      • Hepatic Sinusoidal Obstruction Syndrome May Be Associated with a Sepsis-Like Syndrome with Hypotension
                  • Hypercapnia (see Hypercapnia and Respiratory Failure)
                    • Physiology
                      • Hypercapnia-Associated 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-Associated Cardiovascular Changes
                        • Increased Heart Rate (by 10-20 Beats/Min)
                        • Increased Plasma Volume
                        • Increased Cardiac Output
                        • Increases Stroke Volume
                        • Decreased Blood Pressure
                        • Decreased Pulmonary Vascular Resistance (PVR)
                        • Decreased Systemic Vascular Resistance (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)
                    • Physiology
                      • Peripheral Vasodilation
                    • Clinical
                      • High-Output Heart Failure May Occur
                  • Systemic Mastocytosis (see Systemic Mastocytosis)
                    • Physiology
                      • Peripheral Vasodilation
                  • Vasoplegic Syndrome (Post-Cardiac Surgery Vasodilation) (see Vasoplegic Syndrome)
                    • Physiology
                      • Peripheral Vasodilation Following Cardiac Surgery
                  • Vasovagal Syncope (see Vasovagal Syncope)
                    • Physiology
                      • Peripheral Vasodilation

                      Etiology of Increased Systemic Vascular Resistance (SVR)

                      Endocrinologic

                      • Pheochromocytoma (see Pheochromocytoma)
                        • Physiology
                          • Secretion of Adrenergic Substances

                      Drug/Toxin-Associated Vasoconstriction

                      • Bites/Stings
                        • Widow Spider Bite (see Widow Spider Bite)
                          • Epidemiology
                            • Hypertension is More Characteristically Seen in Widow Spider Bites
                            • Hypotension Occurs Rarely
                      • Caffeine (see Caffeine)
                        • Pharmacology:
                      • Cocaine Intoxication (see Cocaine)
                        • Pharmacology
                          • Vasoconstriction
                      • Dopamine (see Dopamine)
                        • Pharmacology
                          • Vasoconstriction
                      • Methamphetamine Intoxication (see Methamphetamine)
                        • Pharmacology
                          • Vasoconstriction
                      • Norepinephrine (Levophed) (see Norepinephrine)
                        • Pharmacology
                          • Vasoconstriction
                      • Phenylephrine (Neosynephrine) (see Phenylephrine)
                        • Pharmacology
                          • Vasoconstriction
                      • Terbutaline (Brethine) (see Terbutaline)
                        • Pharmacology
                          • XXXXX
                      • Vasopressin (see Vasopressin)
                        • Pharmacology
                          • Vasoconstriction


                      Pulmonary Vascular Resistance (PVR)

                      Calculation of Pulmonary Vascular Resistance (PVR) Using Pressures Measured from Swan-Ganz Catheter (see Swan-Ganz Catheter)

                      • Calculation Technique
                        • Pulmonary Vascular Resistance (PVR) is Calculated from the Mean Arterial Pressure (MAP), Central Venous Pressure (CVP), and Cardiac Output (CO)
                          • Unlike, Pulmonary Vascular Resistance, All Three of These Latter Parameters are Measured
                      • Equation: PVR = [(PA Mean – PCWP)/CO] x 80
                        • Normal PVR Values (using dynes-sec/cm5): 20-120 dynes-sec/cm5
                        • Note: PVR normal values can alternatively be expressed as 0.25–1.6 Woods units (or 0.25–1.6 mm Hg-min/L) -> to convert from Woods units to dynes-sec/cm5, multiply by 80

                      Etiology of Increased Pulmonary Vascular Resistance (PVR)

                      • Very Low Lung Volume/Atelectasis (see Atelectasis)
                        • Mechanism
                          • Capillaries are Compressed, Increasing Pulmonary Vascular Resistance (PVR)
                      • High Lung Volume/High Plateau Pressure (see Acute Respiratory Distress Syndrome)
                        • Mechanism
                          • Capillaries are Stretched (Decreasing Their Caliber), Increasing the Pulmonary Vascular Resistance (PVR)
                      • Hypercapnia (see Hypercapnia)
                        • Mechanism
                          • Pulmonary Vasoconstriction (J Appl Physiol, 2003) [MEDLINE]
                          • Hypercapnic Pulmonary Vasoconstriction May Be Responsive to Nitric Oxide
                          • When Associated with High PEEP in the Setting of ARDS, Hypercapnic Pulmonary Vasoconstriction May Result in RV Dysfunction (Intensive Care Med, 2009) [MEDLINE]
                      • Hypoxemia (see Hypoxemia)
                        • Mechanism
                          • Pulmonary Vasoconstriction
                          • Hypoxic Pulmonary Vasoconstriction is Enhanced by Acidosis
                      • Pulmonary Hypertension (see Pulmonary Hypertension)


                      Central Venous Pressure (CVP)

                      Physiologic Determinants of Central Venous Pressure

                      • Atrial and Ventricular Compliance
                      • Right Ventricular (RV) Function
                      • Venous Return

                      Measurement of Central Venous Pressure (CVP)

                      • Central Venous Pressure is Transduced from the Distal (End) Port of a Central Venous Catheter (CVC) or Peripherally Inserted Central Catheter (PICC) (see Central Venous Catheter and Peripherally Inserted Central Catheter)
                        • Distal Port is Traditionally Located in Either the Superior Vena Cava (or the Right Atrium)

                      Clinical Efficacy Data

                      Clinical Efficacy-Measurement of Central Venous Pressure (CVP) Via a Peripherally Inserted Central Catheter (PICC) (see Peripherally Inserted Central Catheter)

                      • General Comments
                        • Peripherally Inserted Central Catheter (PICC) Has a Longer Length and a Narrower Lumen than a Central Venous Catheter (CVC)
                          • Peripherally Inserted Central Catheter (PICC) has a Higher Intrinsic Resistance than a Central Venous Catheter (CVC)
                        • Central Venous Pressure (CVP) Monitoring is an Indicated Use by Several Commercially Available Peripherally Inserted Central Catheters (PICC’s)
                          • AngioDynamics
                          • Arrow
                          • Bard
                          • Medcomp
                      • Early Study Comparing Central Venous Pressure (CVP) Obtained from Central Venous Catheters (CVC’s) and Peripherally Inserted Central Catheters (PICC’s) (2000) [MEDLINE]: study used 77 data pairs from 12 patients with measurements recorded at end-expiration in 19-gauge double-lumen peripherally inserted central catheters (PICC’s) (zeroed at the right atrium)
                        • Peripherally Inserted Central Catheters (PICC’s) Used in This Study Did Not Have High Infusion Rate Capability
                        • To Overcome the Higher Intrinsic Resistance of the Peripherally Inserted Central Catheter (PICC), a Continuous Infusion Device was Used with Heparinized Saline at 3 mL/hr (as is Commonly Used for Arterial Lines)
                        • Central Venous Pressure (CVP) Recorded from a Peripherally Inserted Central Catheter (PICC) is About 1 mm Hg Higher than that Obtained from Central Venous Pressure (CVP) Recorded from a Central Venous Catheter (CVC) (This Difference is Believed to Be Clinically Insignificant)
                        • Peripherally Inserted Central Catheters (PICC’s) Can Be Used to Measure Central Venous Pressure (CVP), Provided that Continuous Infusion Device is Used with Heparinized Saline
                      • Operative Study During AAA Repair Comparing Central Venous Pressure (CVP) Obtained from Central Venous Catheters (CVC’s) and Peripherally Inserted Central Catheters (PICC’s) (2006) [MEDLINE]
                        • Peripherally Inserted Central Catheters (PICC’s) are an Effective Method for Central Venous Pressure (CVP) Monitoring in Situations of Dynamic Systemic Compliance and Preload, Such as During Elective AAA Repair
                      • In Vitro Study Comparing CVP Obtained from Central Venous Catheters (CVC’s) and Peripherally Inserted Central Catheters (PICC’s) (2010) [MEDLINE]: in vitro study of AngioDynamics Morpheus Peripherally Inserted Central Catheter (PICC)
                        • Unlike Other Peripherally Inserted Central Catheters (PICC) Models, the Morpheus Peripherally Inserted Central Catheter (PICC) Shaft Has a Stiff Proximal End with a Softer Distal End
                          • The Stiff Proximal End Decreases Intraluminal Resistance, Prevents Compression by Soft Tissues Prior to Vessel Entry, and Prevents Compression of the Catheter in Region of the Subclavian Vein (Which is a Known Compression Site for Vascular Catheters)
                        • AngioDynamics Morpheus Peripherally Inserted Central Catheter (PICC) was Equivalent to Central Venous Catheter (CVC) When Measuring Central Venous Pressure (CVP)
                      • Korean Study Utilizing Peripherally Inserted Central Catheter (PICC) and Central Venous Pressure (CVP) Measurements During Liver Transplantation (2011) [MEDLINE]: study using double-lumen Arrow Peripherally Inserted Central Catheter (PICC)
                        • Peripherally Inserted Central Catheter (PICC was a Viable alternative to Central Venous Catheter (CVC) for Central Venous Pressure (CVP) Measurement During Liver Transplantation
                      • In Vitro and In Vivo Study Comparing Central Venous Pressure (CVP) Obtained from Central Venous Catheter (CVC) and Peripherally Inserted Central Catheter (PICC) (2012) [MEDLINE]: study used triple and double-lumen Bard PowerPICC’s (with high infusion rate capability) vs central venous catheter (CVC) in in vitro (540 pressure measurements) and in vivo (70 pressure measurements) protocols
                        • Peripherally Inserted Central Catheter (PICC) was Equivalent to Central Venous Catheter (CVC) When Measuring Central Venous Pressure (CVP) in Intensive Care Unit (ICU) Patients

                      Clinical Efficacy-Utility of Central Venous Pressure (CVP) to Assess Volume Status and Volume Responsiveness

                      • Systematic Review of Clinical Utility of Central Venous Pressure (CVP) (Chest, 2008) [MEDLINE]
                        • Systematic Review of 24 Studies (Which Studied Either the Relationship Between Central Venous Pressure (CVP) and Blood Volume or Reported the Associated Between Central Venous Pressure (CVP)/Delta Central Venous Pressure (CVP) and the Change in Stroke Volume/Cardiac Index Following a Fluid Challenge)
                        • There was a Very Poor Relationship Between Central Venous Pressure (CVP) and Blood Volume, as Well as the Inability of Central Venous Pressure (CVP)/Delta Central Venous Pressure (CVP) to Predict the Hemodynamic Response to a Fluid Challenge
                        • Despite Widely-Used Clinical Guidelines Recommending the Use of Central Venous Pressure (CVP), the Central Venous Pressure (CVP) Should Not Be Used to Make Clinical Decisions Regarding Fluid Management
                      • Meta-Analysis of Central Venous Pressure to Predict Fluid Responsiveness (Crit Care Med, 2013) [MEDLINE]: n= 43 studies (healthy adult controls n = 1, intensive care unit patients n = 22, and operating room patients n = 20)
                        • Overall 57% ± 13% of the Patients were Fluid Responders
                        • Summary Area Under the Curve was 0.56 (95% CI: 0.54-0.58) with No Heterogenicity Between the Studies
                        • Summary Area Under the Curve was 0.56 (95% CI: 0.52-0.60) for Those Studies Done in the Intensive Care Unit and 0.56 (95% CI: 0.54-0.58) for Those Studies Done in the Operating Room
                        • Summary Correlation Coefficient Between the Baseline Central Venous Pressure and Change in Stroke Volume Index/Cardiac Index was 0.18 (95% CI: 0.1-0.25), Being 0.28 (95% CI: 0.16-0.40) in the Intensive Care Unit Patients and 0.11 (95% CI: 0.02-0.21) in the Operating Room Patients
                        • There are No Data to Support the Widespread Practice of Using Central Venous Pressure to Guide Fluid Therapy
                      • Systematic Review Examining CVP in Predicting Fluid Responsiveness in Critically Ill Patients (Intensive Care Med, 2016) [MEDLINE]: n = 1148 (51 studies)
                        • Central Venous Pressure (CVP) was Subgrouped into Low (<8 mmHg), Intermediate (8-12 mmHg), High (>12 mmHg) Baseline Central Venous Pressure (CVP)
                        • Although Authors Identified Some Positive and Negative Predictive Values for Fluid Responsiveness for Specific Low and High Values of Central Venous Pressure (CVP), Respectively, None of the Predictive Values were >66% for Any Central Venous Pressure (CVP) from 0 to 20 mm Hg
                        • Central Venous Pressure (CVP) in the Normal Range Does Not Predict Fluid Responsiveness

                        Recommendations (2016 Surviving Sepsis Guidelines; Intensive Care Med, 2017) [MEDLINE] (Intensive Care Med, 2014) [MEDLINE]

                        • Use of Central Venous Pressure (CVP) Alone to Guide Resuscitation is Not Recommended in Sepsis


                        Pulmonary Capillary Wedge Pressure (PCWP)

                        Measurement Technique

                        Correction of Pulmonary Capillary Wedge Pressure Correction for Applied PEEP


                        Left Atrial End-Diastolic Pressure (LA-EDP)


                        Oxygen Delivery and Consumption

                        Central Venous O2 Saturation (ScvO2)

                        General Comments

                        • Source of ScvO2: SaO2 sampled from SVC, with CVC tip above the RA
                        • Normal ScvO2: 65-80% (usually around 70%)
                          • ScvO2 is Usually Slightly Higher Than the SvO2: as ScvO2 is sampled at a point where venous blood from the coronary sinus has not mixed in yet (however, ScvO2 and SvO2 trend together)

                        Etiology of Increased ScvO2 (Decreased Oxygen Demand or Increased Oxygen Supply)

                        • Cyanide Intoxication (see Cyanide): due to decreased tissue extraction
                        • High pO2
                        • Hypothermia (see Hypothermia): due to decreased tissue metabolic rate
                        • L->R Intracardiac Shunt (see Intracardiac and Extracardiac Shunt): oxygenated blood is shunted from L->R
                        • Sepsis (see Sepsis): due to effective “shunting” with resultant decreased tissue extraction
                        • Severe Mitral Regurgitation (see Mitral Regurgitation,)

                        Etiology of Decreased ScvO2 (Insufficient Oxygen Delivery or Increased Oxygen Demand)

                        Institute for Healthcare Improvement (IHI) Sepsis Goal-Directed Therapy Targets for ScvO2

                        • Target: ScvO2 >70%
                        • Target: CVP >8 (target: CVP>12 in mechanically ventilated patients and those with increased abdominal pressure)
                        • Target: Hct >30

                        Mixed Venous O2 Saturation (SvO2)

                        General Comments

                        • Source of SvO2: SaO2 sampled from Swan-distal port
                        • Normal SvO2: 68-77%
                          • ScvO2 is Usually Slightly Higher Than the SvO2: as ScvO2 is sampled at a point where venous blood from the coronary sinus has not mixed in yet (however, ScvO2 and SvO2 trend together)

                          Etiology of Increased SvO2 (Decreased Oxygen Demand or Increased Oxygen Supply)

                          • Cyanide Intoxication (see Cyanide): due to decreased tissue extraction
                          • High pO2
                          • Hypothermia (see Hypothermia): due to decreased tissue metabolic rate
                          • L->R Intracardiac Shunt (see Intracardiac and Extracardiac Shunt): oxygenated blood is shunted from L->R
                          • Sepsis (see Sepsis): due to effective “shunting” with resultant decreased tissue extraction
                          • Severe Mitral Regurgitation (see Mitral Regurgitation)

                          Etiology of Decreased SvO2 (Insufficient Oxygen Delivery or Increased Oxygen Demand)

                          Institute for Healthcare Improvement (IHI) Sepsis Goal-Directed Therapy Targets for SvO2

                          • Target: SvO2 >65%
                          • Target: CVP >8 (target: CVP>12 in mechanically ventilated patients and those with increased abdominal pressure)
                          • Target: Hct >30

                          Arterial Oxygen Content

                          Most of the Oxygen Which Diffuses from the Alveolus into the Blood is Bound by Hemoglobin

                          • The Amount of Oxygen Dissolved in Plasma is Generally Small Relative to the Amount of Oxygen Bound to Hemoglobin, But Becomes Significant at Very High pO2 (as in a Hyperbaric Chamber) or in Severe Anemia
                            • The Constant 0.0031 in the Arterial Oxygen Content Represents the Amount of Oxygen Dissolved in the Plasma
                            • Because this Amount is Relatively Small, the pO2 Term is Commonly Omitted from the Arterial Oxygen Content Equation (as We Do Below)
                          • Under Normal Conditions, Complete Oxygenation of the Blood Occurs in 0.25 sec (This is Approximately One Third of the Total Time that the Blood is in Contact with the Alveolar-Capillary Membrane)
                            • This Rapid Diffusion Normally Allows the System to Sufficiently Compensate for Any Impairment in Oxygen Diffusion
                          • In Dyshemoglobinemias (Such as Sickle Cell Disease, etc), the Arterial Oxygen Content is Calculated with the Same Equation as Below, Although the Saturations (and Therefore, the Oxygen Content) Will Be Different for a Specific pO2 (Pediatr Pulmonol, 1999) [MEDLINE]

                          Arterial Oxygen Content Equation

                          • Arterial Oxygen Content = [Hb x 13.4 x SaO2 + (0.0031 x pO2)]
                            • Hemoglobin (Hb): in g/dL
                            • Constant 13.4: accounts for the fact that 1.34 ml of O2 is carried per g of Hb (13.4 is used in the equation to correct the units from dL to L)
                            • Arterial Oxygen Saturation (SaO2): as a decimal
                            • pO2: in mm Hg
                            • Normal Arterial Oxygen Content: approximately 200 mL O2/L (or 20 mL O2/dL)
                              • This Equation Will Yield the Arterial Oxygen Content in mL O2/L, Which Allows the Arterial Oxygen Content Value to Be Plugged into the Oxygen Delivery Equation Below without Unit Conversion
                          • Simplified Arterial O2 Content (Omitting the pO2 Term) Arterial O2 Content = [Hb x 13.4 x (SaO2)]

                          Oxygen Delivery Equation

                          • Definition: rate at which oxygen is transported from the lungs to the tissues
                            • Using a Train Analogy
                              • Hb = number of boxcars
                              • SaO2= how full the boxcars are
                              • CO = how fast the train is going
                          • O2 Delivery = CO x Arterial O2 Content x 10 = CO x [Hb x 1.34 x SaO2] x 10
                            • CO: in L/min
                            • Hb: in g/dL
                            • SaO2: as decimal
                            • Factor of 10 in the Equation Converts Everything to mL
                            • Normal (Using Cardiac Output): 1000 mL/min
                            • Normal (Using Cardiac Index): 500 mL/min/m2

                          Oxygen Consumption Equation

                          • Oxygen Consumption = CO x [Hb x 1.34 x (SaO2-SvO2)]
                            • Hb: in g/dL
                            • SaO2: as decimal
                            • SvO2: as decimal
                            • Normal (Using Cardiac Output): 250 mL/min
                            • Normal (Using Cardiac Index): 110-130 mL/min/m2

                          Fick Equation

                          • Fick Cardiac Output = Oxygen Consumption/(10 x Arteriovenous O2 Difference)
                          • Fick Cardiac Output = Oxygen Consumption/(10 x Arterial Oxygen Content – Venous Oxygen Content)
                          • Fick Cardiac Output = 250/[(Hb x 13.4 x SaO2) – (Hb x 13.4 x SvO2)]
                            • Oxygen Consumption: this equation assumes the oxygen consumption is approximately 250 mL/min (or determined by respirometry or a nomogram)
                            • Arteriovenous O2 Difference: in mL O2/dL
                            • Hemoglobin (Hb): in g/dL
                            • Arterial Oxygen Saturation (SaO2): as a decimal
                            • Venous Oxygen Saturation (SaO2): as a decimal

                          Oxygen Extraction Ratio

                          • Oxygen Extraction Ratio = [O2 Consumption/O2 Delivery] x 100
                            • Normal: 23-32% (interpretation: only 20-30% of oxygen delivered is taken up by tissues)
                          • Etiology of Increased Oxygen Extraction Ratio
                            • Low Cardiac Output State
                              • Cardiogenic Shock
                              • Hypovolemic Shock
                          • Etiology of Decreased Oxygen Extraction Ratio
                            • Sepsis (see Sepsis): due to peripheral shunting and decreased tissue extraction
                            • Hepatopulmonary Syndrome (see Hepatopulmonary Syndrome): due to high CO + low SVR state seen in cirrhosis


                          Hemodynamic Patterns

                          High Cardiac Output + Low Systemic Vascular Resistance Pattern (with Normal Pulmonary Capillary Wedge Pressure and Central Venous Pressure)

                          Conditions with Predominant Peripheral Vascular Effects

                          Conditions with Predominant Metabolic Effects

                          • Hyperthyroidism (see Hyperthyroidism)
                          • Myeloproliferative Disorders with Extramedullary Hematopoiesis

                          Conditions with Myocardial and Peripheral Vascular Effects

                          Other

                          • Anaphylaxis (see Anaphylaxis)
                          • Anemia (Chronic, Severe) (see Anemia)
                          • Chronic Pulmonary Disease (with Hypoxemia and/or Hypercapnia)
                          • Exercise
                          • Fever (see Fever)
                          • Hot Climate
                          • Pregnancy (see Pregnancy)

                            Equalization of Central Venous Pressure + Right Ventricular-Diastolic + Pulmonary Artery-Diastolic + Pulmonary Capillary Wedge Pressure

                            “Right Ventricular Restrictive” Pattern (Equalization of Central Venous Pressure/Right Ventricular-Diastolic/Pulmonary Artery-Diastolic + Low-Normal Pulmonary Capillary Wedge Pressure)

                            • Right Ventricular Infarct (see Coronary Artery Disease)
                              • Right Ventricular Infarct Occurs in Association with Inferior Wall Myocardial Infarction

                            Hypovolemic/Hemorrhagic Shock Pattern = Low Central Venous Pressure + Low Pulmonary Capillary Wedge Pressure + Low Cardiac Output + High Systemic Vascular Resistance

                            Cor Pulmonale Pattern = High Central Venous Pressure + Normal Pulmonary Capillary Wedge Pressure + Low Cardiac Output + High Pulmonary Vascular Resistance

                            Left Heart Failure Pattern = High Central Venous Pressure + High Pulmonary Capillary Wedge Pressure + Low Cardiac Output + Normal Pulmonary Vascular Resistance

                            SaO2 “Step-Up” of >5% from Right Atrium to Pulmonary Artery

                            Large v-Waves on Pulmonary Capillary Wedge Pressure Tracing


                            References

                            General

                            Mean Arterial Pressure

                            Cardiac Output

                            Pulmonary Capillary Wedge Pressure

                            Central Venous Pressure (CVP)

                            Ultrasound