Hemodynamics

Blood Pressure

Blood Pressure Measurement Technique

  • Sphygmomanometer (see Sphygmomanometer)
    • Allows Nonivasive Measurement of Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP)
    • Nonivasive 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 = (SBP-DBP)/(3 + DBP)
    • 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 of the Swan-Ganz Catheter, Followed by Use of the 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% (Thus, 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)

Equations

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

Etiology of Decreased Cardiac Output (Cardiogenic Shock) (see Cardiogenic Shock)

Arrhythmia/Conduction Disturbance

Cardiomyopathy (see Congestive Heart Failure)

  • Primary Cardiomyopathies (Predominantly Involving the Heart)
  • Secondary Cardiomyopathies

Increased Afterload

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

Valvular Heart Disease/Cardiac Mechanical Disturbance/Intracardiac Shunt

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

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

Mechanical
  • Abdominal Compartment Syndrome (see Abdominal Compartment Syndrome)
    • Physiology
      • Decreased Venous Return to Right Side of Heart
      • Impaired Myocardial Contractility
  • Aortocaval Compression (Due to Positioning or Surgical Retraction)
    • Physiology
      • Caval Compression, Resulting in Decreased Venous Return to Right Side of Heart
      • Aortic Compression, Resulting in Increased Left Ventricular Afterload
  • Dynamic Hyperinflation (Severe)
    • Positive End-Expiratory Pressure (PEEP)/Auto-PEEP (see Invasive Mechanical Ventilation-General)
      • Physiology
        • Increased Intrathoracic Pressure, Resulting in Decreased Venous Return to Right Side of Heart
  • Hemothorax (Large) (see Pleural Effusion-Hemothorax)
    • Physiology
      • Increased Intrathoracic Pressure with Mass Effect on the Mediastinum (with Compression of Heart and Great Vessels) and the Contralateral Lung
  • Herniation of Abdominal Viscera Into the Thorax
    • Physiology
      • Increased Intrathoracic Pressure, Resulting in Decreased Venous Return to the Right-Side of the Heart
  • Positive-Pressure Ventilation with High Airway Pressures (see Acute Respiratory Distress Syndrome)
    • Physiology
      • Increased Intrathoracic Pressure, Resulting in Decreased Venous Return to the Right Side of Heart
  • Tension Pneumothorax (see Pneumothorax)
    • Physiology
      • Increased Intrathoracic Pressure with Mass Effect on the Mediastinum (with Compression of Heart and Great Vessels) and the Contralateral Lung
Pulmonary Vascular
  • Acute or Severe Pulmonary Hypertension (see Pulmonary Hypertension)
    • General Comments: abrupt/severe increase in pulmonary pressure (i.e. increased pulmonary vascular resistance) results in right-sided heart failure (which may subsequently impair left ventricular filling)
    • Acute Pulmonary Embolism (PE) (see Acute Pulmonary Embolism)
      • Physiology
        • Mechanical Obstruction of Pulmonary Vasculature by Embolism
        • Pulmonary Vasoconstriction (Due to Release of Serotonin and Thromboxane) (Cardiovascular Res, 2000) [MEDLINE]
    • Chronic Thromboembolic Pulmonary Hypertension (CTEPH) (see Chronic Thromboembolic Pulmonary Hypertension)
      • Physiology
        • Mechanical Obstruction of Pulmonary Vasculature
    • Idiopathic Pulmonary Arterial Hypertension (IPAH) (see Idiopathic Pulmonary Arterial Hypertension)
      • Physiology
        • Pulmonary Vascular Smooth Muscle Proliferation and Vasoconstriction
    • Other Causes of Severe Pumonary Hypertension
  • Venous Air Embolism (see Air Embolism)
    • Physiology
      • Venous Air Embolized to the Pulmonary Vasculature in a Sufficient Amount to Obstruct Pulmonary Arterial Blood Flow

Etiology of Increased Cardiac Output

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 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 May Occur in Some Cases (But Heart Failure with Right Heart Valvular Fibrosis is a More Common Cardiac Presentation)
  • Cirrhosis/Liver Disease (see Cirrhosis)
    • Physiology
      • Progressive Systemic Vasodilation (Especially Splanchnic)
      • Development of Intrahepatic/Mesenteric Arteriovenous Shunts
    • 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)
    • Epidemiology
      • Includes Psoriasis, Drug Hypersensitivity Reaction, etc
    • Physiology
      • Significant Cutaneous Vasodilation and Increased Blood Flow to 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]
    • Clinical
      • High Cardiac Output (Although it is Normal When Adjusted for Body Weight)
  • Systemic Arteriovenous Fistula (see Systemic Arteriovenous Fistula)
    • 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
    • Clinical

Systemic Vascular Resistance (SVR)

  • Calculation Technique: SVR is calculated from the MAP, CVP, and CO (all three of these 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)

Septic Shock

  • Sepsis/Severe Sepsis/Septic Shock (see Sepsis)

Systemic Inflammatory Response Syndrome (SIRS) (see Sepsis)

Anaphylaxis/Anaphylactic Shock

Endocrine/Nutritional Deficiency-Associated Hypotension

Hematologic Disease-Associated Hypotension

Neurogenic Shock (see Neurogenic Shock)

Drug/Toxin-Associated Hypotension

Other

  • Cirrhosis/End-Stage Liver Disease (see Cirrhosis): typically results in a high CO/low SVR state
  • Hepatic Veno-Occlusive Disease (see Hepatic Veno-Occlusive Disease)
  • 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)
    • Epidemiology
      • 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)
  • Vasovagal Episode (see Vasovagal Episode)

Etiology of Increased Systemic Vascular Resistance (SVR)

Drug/Toxin-Associated Vasoconstriction

Pulmonary Vascular Resistance (PVR)

  • Calculation Technique: PVR is calculated from the PA-Mean, PCWP, and CO (all three of these 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 PVR
  • High Lung Volume/High Plateau Pressure (see Acute Respiratory Distress Syndrome)
    • Mechanism: capillaries are stretched (decreasing their caliber), increasing 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)

Determinants of Central Venous Pressure

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

Measurement of Central Venous Pressure

General Comments

  • Source of CVP Measurement: measured from right atrium or superior vena cava

Measurement with Central Venous Catheter (CVC) (see Central Venous Catheter)

  • Technique: distal (end) port pressure monitoring is utilized routinely to measure CVP

Measurement with Peripherally Inserted Central Catheter (PICC) (see Peripherally Inserted Central Catheter)

  • General Comments
    • PICC lines have longer length and narrower lumen than CVC’s -> PICC has higher intrinsic resistance than CVC
    • CVP monitoring is an indicated use by several commercially available PICC’s (AngioDynamics, Arrow, Bard, Medcomp)
  • Early Study Comparing CVP Obtained from CVC and PICC Lines (2000) [MEDLINE]
    • Study: 77 data pairs from 12 patients with measurements recorded at end-expiration in 19-gauge double-lumen PICC’s (zeroed at right atrium)
      • PICC’s used in this study did not have high infusion rate capability
      • To overcome the higher inherent resistance of the PICC, a continuous infusion device was used with heparinized saline at 3 mL/hr (as in arterial lines)
    • Main Findings: CVP recorded from a PICC line is about 1 mm Hg higher than CVP recorded from a CVC (this difference is believed to be clinically insignificant) -> PICC lines can be used to measure CVP, provided that continuous infusion device is used with heparinized saline
  • Operative Study During AAA Repair Comparing CVP Obtained from CVC and PICC Lines (2006) [MEDLINE]
    • Main Findings: PICCs are an effective method for CVP monitoring in situations of dynamic systemic compliance and preload, such as during elective AAA repair
  • In Vitro Study Comparing CVP Obtained from CVC and PICC Lines (2010) [MEDLINE]
    • Study: in vitro study of AngioDynamics Morpheus PICC
      • Unlike other PICC models, the Morpheus PICC shaft has a stiff proximal end with a softer distal end: stiff proximal end decreases intraluminal resistance, prevents compression by soft tissues prior to vessel entry, and prevents compression of catheter in region of the subclavian vein (which is a known compression site for vascular catheters)
    • Main Findings: PICC was equivalent to CVC when measuring CVP
  • Korean Study Utilizing PICC and CVP Measurements During Liver Transplantation (2011) [MEDLINE]
    • Study: double-lumen Arrow PICC
    • Main Findings: PICC was a viable alternative to CVC for CVP measurement during liver transplantation
  • In Vitro and In Vivo Study Comparing CVP Obtained from CVC and PICC Lines (2012) [MEDLINE]
    • Study: used triple and double-lumen Bard PowerPICC’s (with high infusion rate capability) vs CVC in in vitro (540 pressure measurements) and in vivo (70 pressure measurements) protocols
    • Main Findings: PICC was equivalent to CVC when measuring CVP in ICU patients

Clinical Utility of Central Venous Pressure to Assess Volume Status and Volume Responsiveness

  • Systematic Review of Clinical Utility of CVP (2008) [MEDLINE]
    • Study: systematic review of 24 studies (which studied either the relationship between CVP and blood volume or reported the associated between CVP/DeltaCVP and the change in stroke volume/cardiac index following a fluid challenge)
    • Main Findings: very poor relationship between CVP and blood volume, as well as the inability of CVP/DeltaCVP to predict the hemodynamic response to a fluid challenge
    • Conclusions: despite widely-used clinical guidelines recommending the use of CVP, the CVP should not be used to make clinical decisions regarding fluid management
  • Systematic Review Examining CVP in Predicting Fluid Responsiveness in Critically Ill Patients (Intensive Care Med, 2016) [MEDLINE]: n = 1148 (51 studies)
    • CVP was Subgrouped into Low (<8 mmHg), Intermediate (8-12 mmHg), High (>12 mmHg) Baseline CVP
    • Although Authors Identified Some Positive and Negative Predictive Values for Fluid Responsiveness for Specific Low and High Values of CVP, Respectively, None of the Predictive Values were >66% for Any CVP from 0 to 20 mm Hg
    • CVP in the Normal Range (Especially in the -12 mm Hg Range) Does Not Predict Fluid Responsiveness

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

  • Use of CVP Alone to Guide Resuscitation is Not Recommended in Sepsis

Pulmonary Capillary Wedge Pressure (PCWP)

Measurement Technique

  • PCWP is Measured from the Swan-Ganz Catheter with the Balloon Inflated and “Wedged” in a Pulmonary Artery Branch (see Swan-Ganz Catheter)
    • By Convention, PCWP is Measured at End-Expiration, Where the Extravascular (i.e. Pleural Pressure) is Zero
      • Assuming Passive Inspiration/Expiration (Indicated by a Zero Slope of the PCWP Waveform) in a Spontaneously-Breathing Patient, End-Expiration Occurs at the “Peak” of the PCWP Waveform
      • Assuming Passive Inspiration/Expiration (Indicated by a Zero Slope of the PCWP Waveform) in a Mechanically-Ventilated Patient, End-Expiration Occurs in the “Valley” of the PCWP Waveform (“Vent = Valley”)
      • In a Patient Who is Actively Expiring, PCWP Waveform Will Have a Positive (Upward) Slope: in this case, it is impossible to determine an accurate PCWP without an esophageal balloon to measure the actual pleural pressure (since pleural pressure is not zero at end-expiration)
  • Using the Airway Pressure Tracing to Correctly Identify End-Expiration, at Which the Pulmonary Capillary Wedge Pressure Should Be Measured
    • Study Attempting to Improve Inter-Observer Agreement of PCPW Readings Using Airway Pressure in ARDS (Crit Care Med, 2005) [MEDLINE]
      • When Using a Standard Protocol Using Airway Pressure to Identify End-Expiration in the Tracing, PCWP Reading Agreement (within 2 mm Hg) Improved from 71% without Use of the Airway Pressure to 83% with Use of the Airway Pressure
      • Inter-Observer Agreement was Higher for Strips Demonstrating >8 mm Hg in Phasic Respiratory Variation

Correction of Pulmonary Capillary Wedge Pressure Correction for Applied PEEP

  • Change Units of PEEP to mm Hg by Dividing the Amount by 1.3
  • Correct by Subtracting 33-50% of PEEP from the PCWP

Left Atrial End-Diastolic Pressure (LA-EDP)

  • Measurement Technique: measured with (left-sided) cardiac catheterization
    • Normal: 5-12 mm Hg

Oxygen Delivery and Consumption

Central Venous O2 Saturation (ScvO2)

  • 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 (Deceased 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

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

Mized Venous O2 Saturation (SvO2)

  • 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 (Deceased 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)

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 O2 Content

  • Definition: arterial oxygen content is the amount of oxygen bound to hemoglobin + the amount of oxygen dissolved in the arterial blood
  • Arterial O2 Content = [Hb x 1.34 x SaO2 x (0.0031 x pO2)] = [Hb x 1.34 x SaO2]
    • Hb: in g/dL
    • SaO2: as decimal
    • Note: 1.34 ml of O2 is carried per g of Hb
    • Normal: 16-20 mL/dL (16-20 mL O2/dL)
  • Calculation of Arterial O2 Content in Patient with Dyshemoglobinemia (Sickle Cell Disease, etc): same equation is utilized, but the oxygen saturation (and arterial oxygen content) will be different for a specific pO2 (Pediatr Pulmonol, 1999) [MEDLINE]

Oxygen Delivery

  • 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

Arterial-Venous O2 Difference

  • A-V O2 Difference = [Hb x 1.34 x (SaO2-SvO2)]
    • Hb: g/dL
    • SaO2: as decimal
    • SvO2: as decimal
  • Etiology of Increased A-V O2 Difference
    • Low Cardiac Output State
      • Cardiogenic Shock
      • Hypovolemic Shock
  • Etiology of Decreased A-V O2 Difference
    • 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

Oxygen Consumption

  • 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

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, [[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 CO + Low SVR Pattern (with normal PCWP and CVP)

Equalization of CVP + RV-Diastolic + PA-Diastolic + PCWP

“RV Restrictive” Pattern (Equalization of CVP/RV-Diastolic/PA-Diastolic + Low-Normal PCWP)

Hypovolemic/Hemorrhagic Shock Pattern = Low CVP + Low PCWP + Low CO + High SVR

Cor Pulmonale Pattern = High CVP + Normal PCWP + Low CO + High PVR

Left Heart Failure Pattern = High CVP + High PCWP + Low CO + Normal PVR

SaO2 “Step-Up” of >5% from RA -> PA

Large v-Waves on PCWP Tracing

References

General

  • Plasma volume expansion in surgical patients with high central venous pressure: the relationship of blood volume to hematocrit, CVP, pulmonary wedge pressure and cardiorespiratory changes. Surg 1975;78:304-315
  • Critical level of oxygen delivery in anesthetized man. Crit Care Med 1983; 11:640
  • The effects of dopamine on cardiopulmonary function and left ventricular volumes in patients with acute respiratory failure. Am Rev Respir Dis 1984;130:396-399
  • Critical level of oxygen delivery after cardiopulmonary bypass. Crit Care Med 1987; 15:194
  • Measurement of hemoglobin saturation by oxygen in children and adolescents with sickle cell disease. Pediatr Pulmonol. 1999;28(6):423 [MEDLINE]
  • Human pulmonary vascular response to 4 h of hypercapnia and hypocapnia measured using Doppler echocardiography. J Appl Physiol 2003, 94:1543-1551 [MEDLINE]
  • Impact of acute hypercapnia and augmented positive end-expiratory pressure on right ventricle function in severe acute respiratory distress syndrome. Intensive Care Med 2009, 35:1850-1858 [MEDLINE]
  • Pulmonary vascular and right ventricular dysfunction in adult critical care: current and emerging options for management: a systematic literature review. Crit Care. 2010;14(5):R169 [MEDLINE]
  • Hemodynamic Monitoring for the Evaluation and Treatment of Shock: What Is the Current State of the Art? Semin Respir Crit Care Med. 2015 Dec;36(6):890-8. doi: 10.1055/s-0035-1564874. Epub 2015 Nov 23 [MEDLINE]

Pulmonary Capillary Wedge Pressure

  • Effect of airway pressure display on interobserver agreement in the assessment of vascular pressures in patients with acute lung injury and acute respiratory distress syndrome. Crit Care Med. 2005 Jan;33(1):98-103; discussion 243-4 [MEDLINE]

Central Venous Pressure (CVP)

  • Central venous pressure measurements: peripherally inserted catheters versus centrally inserted catheters. Crit Care Med. 2000 Dec;28(12):3833-6 [MEDLINE]
  • Intraoperative peripherally inserted central venous catheter central venous pressure monitoring in abdominal aortic aneurysm reconstruction. Ann Vasc Surg. 2006 Sep;20(5):577-81. Epub 2006 Jul 27 [MEDLINE]
  • Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest. 2008 Jul;134(1):172-8. doi: 10.1378/chest.07-2331 [MEDLINE]
  • An in vitro study comparing a peripherally inserted central catheter to a conventional central venous catheter: no difference in static and dynamic pressure transmission. BMC Anesthesiol. 2010 Oct 12;10:18. doi: 10.1186/1471-2253-10-18 [MEDLINE]
  • Comparison of the central venous pressure from internal jugular vein and the pressure measured from the peripherally inserted antecubital central catheter (PICCP) in liver transplantation recipients. Korean J Anesthesiol. Oct 2011; 61(4): 281–287. Published online Oct 22, 2011. doi: 10.4097/kjae.2011.61.4.281 [MEDLINE]
  • Peripherally inserted central catheters are equivalent to centrally inserted catheters in intensive care unit patients for central venous pressure monitoring. J Clin Monit Comput. 2012 Apr;26(2):85-90. doi: 10.1007/s10877-012-9337-1 [MEDLINE]
  • Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Med 2014; 40(12):1795–1815 [MEDLINE]
  • Systematic review including re‐analyses of 1148 individual data sets of central venous pressure as a predictor of fluid responsiveness. Intensive Care Med 2016, 42(3):324–332 [MEDLINE]
  • Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Med. 2017 Jan 18. doi: 10.1007/s00134-017-4683-6 [MEDLINE]

Ultrasound

  • The respiratory variation in inferior vena cava diameter as a guide to fluid therapy. Intensive Care Med. 2004 Sep;30(9):1834-7. Epub 2004 Mar 25 [MEDLINE]
  • Bedside ultrasonography for the intensivist. Crit Care Clin. 2015 Jan;31(1):43-66. doi: 10.1016/j.ccc.2014.08.003. Epub 2014 Oct 3 [MEDLINE]