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)

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)

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

Measurement of Central Venous Pressure

General Comments

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

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

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

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

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)

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

Etiology of Decreased ScvO2: insufficient oxygen delivery or increased oxygen demand

IHI Sepsis Goal-Directed Therapy Targets for ScvO2

Mized Venous O2 Saturation (SvO2)

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

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

IHI Sepsis Goal-Directed Therapy Targets for SvO2

Arterial O2 Content

Oxygen Delivery

Arterial-Venous O2 Difference

Oxygen Consumption

Oxygen Extraction Ratio

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

Pulmonary Capillary Wedge Pressure

Central Venous Pressure (CVP)

Ultrasound