Hemodynamics

Mean Arterial Pressure (MAP)

  • Measurement/Calculation Technique
    • Sphygmomanometer (see Sphygmomanometer, [[Sphygmomanometer]]): allows measurement of systolic and diastolic blood pressure
    • Arterial Lineb (see Arterial Line, [[Arterial Line]]): allows measurement of systolic and diastolic blood pressure
  • Equation: MAP = (SBP-DBP)/(3 + DBP)
    • Normal: 85-95 mm Hg

Cardiac Output (CO)

  • Measurement/Calculation Techniques
    • Thermodilution Cardiac Output: allows measurement of CO using cold saline injection and Swan-Ganz catheter thermistor (see Swan-Ganz Catheter, [[Swan-Ganz Catheter]])
    • Fick Cardiac Output: Fick CO = O2 Consumption/(10 x A-V O2 Diff)
      • O2 Consumption (Estimated) Can Be Obtained from a Nomogram Which Utilizes Age, Sex, Height, and Weight
      • O2 Consumption Can Also Be Determined Using Breath Analysis
    • FloTrac (see FloTrac, [[FloTrac]]): via arterial line (see Arterial Line, [[Arterial Line]]) and Vigileo monitor
  • Equation: CO = SV x HR
    • Stroke Volume (SV) = (LV-EF x LV-EDV) – Mitral Regurgitation

Etiology of Decreased Cardiac Output (Cardiogenic Shock) (see Cardiogenic Shock, [[Cardiogenic Shock]])

Acute or Severe Pulmonary Hypertension (see Pulmonary Hypertension, [[Pulmonary Hypertension]])

Arrhythmia/Conduction Disturbance

Cardiomyopathy (see Congestive Heart Failure, [[Congestive Heart Failure]])

  • Infection
    • Hantavirus Pulmonary Syndrome (see Hantavirus, [[Hantavirus]]): unusually produces sepsis with a high SVR and low CO state
    • Myocarditis (see Myocarditis, [[Myocarditis]])
    • Sepsis-Induced Myocardial Depression (see Sepsis, [[Sepsis]])
  • Endocrine/Metabolic Disturbance
  • Myocardial Ischemia/Infarction
    • Acute Myocardial Infarction (MI) (see Coronary Artery Disease, [[Coronary Artery Disease]]): involving >40% of left ventricular myocardium
    • Myocardial Ischemia/Stunned Myocardium
  • Post-Cardiopulmonary Bypass (see Cardiopulmonary Bypass, [[Cardiopulmonary Bypass]])
  • Restrictive Cardiomyopathy (see Restrictive Cardiomyopathy, [[Restrictive Cardiomyopathy]])
  • Trauma
  • Takotsubo Cardiomyopathy (Stress-Induced Cardiomyopathy) (see Takotsubo Cardiomyopathy, [[Takotsubo Cardiomyopathy]])
  • Tamponade (see Tamponade, [[Tamponade]]): produces diastolic dysfunction
  • Drugs/Toxins
    • Antiarrhythmics
    • Beta Blockers (see β-Adrenergic Receptor Antagonists, [[β-Adrenergic Receptor Antagonists]]): particularly in the setting of intoxication
    • Calcium Channel Blockers (see Calcium Channel Blockers, [[Calcium Channel Blockers]]): particularly in the setting of intoxication
    • Propofol Infusion Syndrome (see Propofol, [[Propofol]])

Increased Afterload

Increased Intrathoracic Pressure (with Impaired Right-Sided Venous Return)

  • Herniation of Abdominal Viscera Into Thorax
  • Positive-Pressure Ventilation with High Airway Pressures (see Acute Respiratory Distress Syndrome, [[Acute Respiratory Distress Syndrome]])
  • Tension Pneumothorax (see Pneumothorax, [[Pneumothorax]])

Intracardiac Shunt (see Intracardiac and Extracardiac Shunt, [[Intracardiac and Extracardiac Shunt]])

Valvular Disease/Mechanical Disturbance

Etiology of Increased Cardiac Output

  • Anemia (see Anemia, [[Anemia]])
  • Anxiety (see Anxiety, [[Anxiety]])
  • Carcinoid Syndrome (see Carcinoid Syndrome, [[Carcinoid Syndrome]])
    • Clinical: high output heart failure may occur
  • Chronic Kidney Disease (CKD) (see Chronic Kidney Disease, [[Chronic Kidney Disease]])
    • Clinical: high output heart failure may occur
  • Exercise
  • Fever (see Fever, [[Fever]])
  • Hyperthyroidism (see Hyperthyroidism, [[Hyperthyroidism]])
    • Clinical: high output heart failure may occur
  • Cirrhosis/Liver Disease (see Cirrhosis, [[Cirrhosis]])
    • Clinical: high output heart failure may occur
  • Multiple Myeloma (see Multiple Myeloma, [[Multiple Myeloma]])
    • Clinical: high output heart failure may occur
  • Obesity (see Obesity, [[Obesity]])
    • Clinical: high output heart failure may occur
  • Paget Disease of Bone (see Paget Disease of Bone, [[Paget Disease of Bone]])
    • Clinical: high output heart failure may occur
  • Pregnancy (see Pregnancy, [[Pregnancy]]): characteristically produces a high cardiac output/low SVR state (with increased blood volume)
  • Psoriasis (see Psoriasis, [[Psoriasis]])
    • Clinical: high output heart failure may occur
  • Sepsis (see Sepsis, [[Sepsis]])
    • Clinical: high output heart failure may occur
  • Stress
  • Systemic Arteriovenous Fistula (see Systemic Arteriovenous Fistula, [[Systemic Arteriovenous Fistula]])
    • Epidemiology: femoral arteriovenous fistula is the most common types of acquired arteriovenous fistula (due to the frequency of using the femoral site for percutaneous arterial or venous access)
    • Clinical: high output heart failure may occur
  • Thiamine Deficiency (see Thiamine, [[Thiamine]])
    • Clinical: high output heart failure may occur

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

SVRPVR

Etiology of Decreased Systemic Vascular Resistance (Distributive Shock)

Septic Shock

  • Sepsis/Severe Sepsis/Septic Shock (see Sepsis, [[Sepsis]])

Systemic Inflammatory Response Syndrome (SIRS) (see Sepsis, [[Sepsis]])

Anaphylaxis/Anaphylactic Shock

Endocrine/Nutritional Deficiency-Associated Hypotension

Hematologic Disease-Associated Hypotension

Neurogenic Shock (see Neurogenic Shock, [[Neurogenic Shock]])

Drug/Toxin-Associated Hypotension

  • Abacavir-Hypersensitivity Reaction (see Abacavir, [[Abacavir]])
  • All-Trans Retinoic Acid (ATRA)/Retinoic Acid Syndrome (see All-Trans Retinoic Acid, [[All-Trans Retinoic Acid]])
  • Amiodarone (see Amiodarone, [[Amiodarone]])
  • Angiotensin Converting Enzyme (ACE) Inhibitors (see Angiotensin Converting Enzyme (ACE) Inhibitors, [[Angiotensin Converting Enzyme Inhibitors]])
    • Captopril (Capoten) (see Captopril, [[Captopril]])
    • Enalapril (Vasotec, Enalaprilat) (see Enalapril, [[Enalapril]])
    • Fosinopril (Monopril) (see Fosinopril, [[Fosinopril]])
    • Lisinopril (Zestril) (see Lisinopril, [[Lisinopril]])
    • Moexipril (Univasc) (see Moexipril, [[Moexipril]])
    • Perindopril (Coversyl, Coversum, Preterax, Aceon) (see Perindopril, [[Perindopril]])
    • Quinapril (Accupril) (see Quinapril, [[Quinapril]])
    • Ramipril (Altace) (see Ramipril, [[Ramipril]])
    • Trandolapril (Mavik) (see Trandolapril, [[Trandolapril]])
  • Angiotensin II Receptor Blockers (ARB) (see Angiotensin II Receptor Blockers, [[Angiotensin II Receptor Blockers]])
    • Candesartan (Atacand) (see Candesartan, [[Candesartan]])
    • Fimasartan (Kanarb) (see Fimasartan, [[Fimasartan]])
    • Irbesartan (Avapro, Aprovel, Karvea) (see Irbesartan, [[Irbesartan]])
    • Losartan (Cozaar) (see Losartan, [[Losartan]])
    • Olmesartan (Benicar, Olmecip) (see Olmesartan, [[Olmesartan]])
    • Telmisartan (Micardis) (see Telmisartan, [[Telmisartan]])
    • Valsartan (Diovan) (see Valsartan, [[Valsartan]])
  • Atypical Anti-Psychotic Agents
    • Olanzapine (Zyprexa) (see Olanzapine, [[Olanzapine]])
    • Quetiapine (Seroquel) (see Quetiapine, [[Quetiapine]])
    • Risperidone (Risperdal) (see Risperidone, [[Risperidone]])
  • Benzodiazepines (see Benzodiazepines, [[Benzodiazepines]])
    • Alprazolam (Xanax) (see Alprazolam, [[Alprazolam]])
    • Chlordiazepoxide (Librium) (see Chlordiazepoxide, [[Chlordiazepoxide]])
    • Diazepam (Valium) (see Diazepam, [[Diazepam]])
    • Lorazepam (Ativan) (see Lorazepam, [[Lorazepam]])
    • Midazolam (Versed) (see Midazolam, [[Midazolam]])
    • Temazepam (Restoril, Normison) (see Temazepam, [[Temazepam]])
  • Beta Blockers (see β-Adrenergic Receptor Antagonists, [[β-Adrenergic Receptor Antagonists]])
    • Non-Selective Beta Blockers (only selected beta blockers from the category are shown)
      • Nadolol (Corgard, Anabet, Solgol, Corzide, Alti-Nadolol, Apo-Nadol, Novo-Nadolol) (see Nadolol, [[Nadolol]])
      • Propafenone (Rhythmol) (see Propafenone, [[Propafenone]]): with additional Class 1C antiarrhythmic properties (inhibits sodium channels)
      • Propanolol (Inderal) (see Propanolol, [[Propanolol]])
      • Sotalol (Betapace, Betapace AF, Sotalex, Sotacor) (see Sotalol, [[Sotalol]]): with additional Class III antiarrhythmic properties (inhibits potassium channels)
    • Cardioselective (β1-Selective) Beta Blockers (only selected beta blockers from the category are shown)
      • Atenolol (Tenormin) (see Atenolol, [[Atenolol]])
      • Bisoprolol (Concor, Zebeta) (see Bisoprolol, [[Bisoprolol]])
      • Esmolol (Brevibloc) (see Esmolol, [[Esmolol]])
      • Metoprolol (Lopressor) (see Metoprolol, [[Metoprolol]])
      • Nebivolol (Bystolic) (see Nebivolol, [[Nebivolol]])
    • Beta Blockers with Intrinsic Sympathomimetic Activity (β-Adrenergic Receptor Antagonism + Low Level β-Adrenergic Receptor Agonism) (only selected beta blockers from the category are shown)
    • Beta Blockers with Alpha Blocking Activity (only selected beta blockers from the category are shown)
      • Carvedilol (Coreg) (see Carvedilol, [[Carvedilol]])
      • Labetalol (Normodyne, Trandate) (see Labetalol, [[Labetalol]])
  • Calcium Channel Blockers (see Calcium Channel Blockers, [[Calcium Channel Blockers]])
    • Amlodipine (Norvasc) (see Amlodipine, [[Amlodipine]])
    • Diltiazem (Cardizem) (see Diltiazem, [[Diltiazem]])
    • Felodipine (Plendil) (see Felodipine, [[Felodipine]])
    • Isradipine (DynaCirc, Prescal) (see Isradipine, [[Isradipine]])
    • Nicardipine (Cardene) (see Nicardipine, [[Nicardipine]])
    • Nifedipine (Procardia) (see Nifedipine, [[Nifedipine]])
    • Nimodipine (Nimotop) (see Nimodipine, [[Nimodipine]])
    • Verapamil (Calan, Isoptin, Verelan, Verelan PM, Bosoptin, Covera-HS) (see Verapamil, [[Verapamil]])
  • Carbamate Intoxication (see Carbamates, [[Carbamates]])
  • Carbon Monoxide Intoxication (see Carboxyhemoglobinemia, [[Carboxyhemoglobinemia]]): results in mitochondrial dysfunction
  • Cigua Toxin Poisoning (see Cigua Toxin Poisoning, [[Cigua Toxin Poisoning]])
  • Cyanide Intoxication (see Cyanide, [[Cyanide]]): results in mitochondrial dysfunction -> hypotension occurs late in course
  • Cytokine Release Syndrome (see Cytokine Release Syndrome, [[Cytokine Release Syndrome]])
    • Alemtuzumab (Campath, MabCampath, Campath-1H, Lemtrada) (see Alemtuzumab, [[Alemtuzumab]]): anti-CD52 monoclonal antibody
    • TGN1412: anti-CD28 superagonist
    • Anti-Thymocyte Globulin (ATG) (see Anti-Thymocyte Globulin, [[Anti-Thymocyte Globulin]])
    • Basiliximab (Simulect) (see Basiliximab, [[Basiliximab]])
    • Bi-Specific Antibodies in Treatment of Leukemia
    • Haploidentical Mononuclear Cells in Treatment of Refractory Leukemia
    • Lenalidomide (Revlimid) (see Lenalidomide, [[Lenalidomide]])
    • Muromonab-CD3 (Orthoclone OKT3) (see Muromonab-CD3, [[Muromonab-CD3]]): anti-CD3 monoclonal antibody
    • Oxaliplatin (Eloxatin, Oxaliplatin Medac) (see Oxaliplatin, [[Oxaliplatin]])
    • Rituximab (Rituxan) (see Anti-CD20 Therapy, [[Anti-CD20 Therapy]]): chimeric monoclonal anti-CD20 antibody
    • T-Cells Engineered to Express CD19–Chimeric Antigen Receptor (CAR)
  • Dobutamine (Dobutrex) (see Dobutamine, [[Dobutamine]])
    • Pharmacology: vasodilation
  • Endothelin Receptor Antagonists (see Endothelin Receptor Antagonists, [[Endothelin Receptor Antagonists]])
    • Ambrisentan (Letairis) (see Ambrisentan, [[Ambrisentan]])
    • Atrasentan (Xinlay) (see Atrasentan, [[Atrasentan]])
    • Bosentan (Tracleer) (see Bosentan, [[Bosentan]])
    • Macitentan (Opsumit) (see Macitentan, [[Macitentan]])
    • Sitaxentan (Thelin) (see Sitaxentan, [[Sitaxentan]])
    • Tezosentan
    • Zibotentan (see Zibotentan, [[Zibotentan]])
  • Ethylene Glycol Intoxication (see Ethylene Glycol, [[Ethylene Glycol]])
  • Fosphenytoin (Cerebyx) (see Fosphenytoin, [[Fosphenytoin]])
  • Glyphosate Ingestion (see Glyphosate, [[Glyphosate]])
  • Hydralazine (see Hydralazine, [[Hydralazine]])
  • Hydrogen Sulfide Gas Inhalation (see Hydrogen Sulfide Gas, [[Hydrogen Sulfide Gas]])
  • Intravenous Immunoglobulin (IVIG) (see Intravenous Immunoglobulin, [[Intravenous Immunoglobulin]])
  • Isopropanol Intoxication (see Isopropanol, [[Isopropanol]])
  • Metal Intoxication
    • Arsenic Intoxication (see Arsenic, [[Arsenic]])
    • Iron Intoxication (see Iron, [[Iron]])
    • Manganese Intoxication (see Manganese, [[Manganese]])
    • Selenium Intoxication (see Selenium, [[Selenium]])
    • Thallium Intoxication (see Thallium, [[Thallium]])
  • Methanol Intoxication (see Methanol, [[Methanol]])
  • Methemoglobinemia (see Methemoglobinemia, [[Methemoglobinemia]])
  • N-Acetylcysteine (Mucomyst, Acetadote, Fluimucil, Parvolex) (see N-Acetylcysteine, [[N-Acetylcysteine]]): associated with oral administration
  • Nerium Oleander Intoxication (see Nerium Oleander, [[Nerium Oleander]])
  • Opiates (see Opiates, [[Opiates]])
    • Hydromorphone (Dilaudid) (see Hydromorphone, [[Hydromorphone]])
    • Meperidine (Demerol) (see Meperidine, [[Meperidine]])
    • Methadone (Dolophine) (see Methadone, [[Methadone]])
    • Morphine (see Morphine, [[Morphine]])
    • Opiate Intoxication (see Opiates, [[Opiates]])
    • Oxycodone (see Oxycodone, [[Oxycodone]])
  • Organophosphate Intoxication (see Organophosphates, [[Organophosphates]])
  • Phenytoin (Dilantin) (see Phenytoin, [[Phenytoin]])
  • Phosphodiesterase Type 5 (PDE5) Inhibitors (see Phosphodiesterase Type 5 Inhibitors, [[Phosphodiesterase Type 5 Inhibitors]])
    • Sildenafil (Viagra, Revatio) (see Sildenafil, [[Sildenafil]])
    • Tadalafil (Adcirca, Cialis) see Tadalafil, [[Tadalafil]])
    • Vardenafil (Levitra, Staxyn) (see Vardenafil, [[Vardenafil]])
  • Prostaglandins with Vasodilatory Properties
    • Epoprostenol (PGI2, Prostacyclin, Flolan, Veletri) (see Epoprostenol, [[Epoprostenol]])
    • Iloprost (Ilomedin, Ventavis) (see Iloprost, [[Iloprost]])
    • Prostaglandin E1 (Alprostadil) (see Prostaglandin E1, [[Prostaglandin E1]])
  • Protamine (see Protamine, [[Protamine]])
  • Rasburicase (Elitek) (see Rasburicase, [[Rasburicase]])
  • Rattlesnake Bite (see Rattlesnake Bite, [[Rattlesnake Bite]])
  • Salicylate Intoxication (see Acetylsalicylic Acid, [[Acetylsalicylic Acid]])
  • Scombroid (see Scombroid, [[Scombroid]])
  • Scorpion Sting (see Scorpion Sting, [[Scorpion Sting]])
  • Serotonin Syndrome (see Serotonin Syndrome, [[Serotonin Syndrome]])
  • Sevelamer (Renagel, Renvela) (see Sevelamer, [[Sevelamer]])
  • Staphylococcal Toxic Shock Syndrome (see Staphylococcal Toxic Shock Syndrome, [[Staphylococcal Toxic Shock Syndrome]])
  • Streptococcal Toxic Shock Syndrome (see Streptococcal Toxic Shock Syndrome, [[Streptococcal Toxic Shock Syndrome]])
  • Thrombolytics (see Thrombolytics, [[Thrombolytics]])
  • Tocolytic-Induced Pulmonary Edema (see Tocolytic-Induced Pulmonary Edema, [[Tocolytic-Induced Pulmonary Edema]])
  • Transfusion-Associated Acute Lung Injury (TRALI) (see Transfusion-Associated Acute Lung Injury, [[Transfusion-Associated Acute Lung Injury]])
  • Tricyclic Antidepressant Intoxication (see Tricyclic Antidepressants, [[Tricyclic Antidepressants]])
  • Vancomycin-Associated Red Man Syndrome (see Vancomycin, [[Vancomycin]])

Other

  • Arteriovenous Fistula (see Arteriovenous Fistula, [[Arteriovenous Fistula]])
  • Cirrhosis/End-Stage Liver Disease (see Cirrhosis, [[Cirrhosis]]): typically results in a high CO/low SVR state
  • Hepatic Veno-Occlusive Disease (see Hepatic Veno-Occlusive Disease, [[Hepatic Veno-Occlusive Disease]])
  • Pregnancy (see Pregnancy, [[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, [[Purpura Fulminans]])
  • Systemic Mastocytosis (see Systemic Mastocytosis, [[Systemic Mastocytosis]])
  • Vasoplegic Syndrome (Post-Cardiac Surgery Vasodilation) (see Vasoplegic Syndrome, [[Vasoplegic Syndrome]])
  • Vasovagal Episode (see Vasovagal Episode, [[Vasovagal Episode]])

Etiology of Increased Systemic Vascular Resistance (SVR)

Drug/Toxin-Associated Vasoconstriction

  • Cocaine Intoxication (see Cocaine, [[Cocaine]])
    • Physiology: vasoconstriction
  • Dopamine (see Dopamine, [[Dopamine]])
  • Methamphetamine Intoxication (see Methamphetamine, [[Methamphetamine]])
    • Physiology: vasoconstriction
  • Norepinephrine (Levophed) (see Norepinephrine, [[Norepinephrine]])
  • Phenylephrine (Neosynephrine) (see Phenylephrine, [[Phenylephrine]])
  • Vasopressin (see Vasopressin, [[Vasopressin]])

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

SVRPVR

Etiology of Increased Pulmonary Vascular Resistance (PVR)

  • Very Low Lung Volume/Atelectasis (see Atelectasis, [[Atelectasis]])
    • Mechanism: capillaries are compressed, increasing PVR
  • High Lung Volume/High Plateau Pressure (see Acute Respiratory Distress Syndrome, [[Acute Respiratory Distress Syndrome]])
    • Mechanism: capillaries are stretched (decreasing their caliber), increasing PVR

PVR VS LUNG VOL

  • Hypercapnia (see Hypercapnia, [[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, [[Hypoxemia]])
    • Mechanism: pulmonary vasoconstriction
      • Hypoxic Pulmonary Vasoconstriction is Enhanced by Acidosis
  • Pulmonary Hypertension (see Pulmonary Hypertension, [[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, [[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, [[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: measured from Swan-Ganz catheter (see Swan-Ganz Catheter, [[Swan-Ganz Catheter]])
  • 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 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, [[Cyanide]]): due to decreased tissue extraction
  • High pO2
  • Hypothermia (see Hypothermia, [[Hypothermia]]): due to decreased tissue metabolic rate
  • L->R Intracardiac Shunt (see Intracardiac and Extracardiac Shunt, [[Intracardiac and Extracardiac Shunt]]): oxygenated blood is shunted from L->R
  • Sepsis (see Sepsis, [[Sepsis]]): due to effective “shunting” with resultant decreased tissue extraction
  • Severe Mitral Regurgitation (see Mitral Regurgitation, [[Mitral Regurgitation]])

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

  • Low Cardiac Output States
    • Cardiogenic Shock
    • Hypovolemic Shock
  • R->L Intracardiac Shunt (see Intracardiac and Extracardiac Shunt, [[Intracardiac and Extracardiac Shunt]]): deoxygenated blood is shunted from R->L

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

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

  • Low Cardiac Output State
    • Cardiogenic Shock
    • Hypovolemic Shock
  • R->L intracardiac shunt (see Intracardiac and Extracardiac Shunt, [[Intracardiac and Extracardiac Shunt]]): deoxygenated blood is shunted from R->L

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

OXYGEN DELIVERY

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, [[Sepsis]]): due to peripheral shunting and decreased tissue extraction
    • Hepatopulmonary Syndrome (see Hepatopulmonary Syndrome, [[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, [[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)

  • RV Infarct (see Coronary Artery Disease, [[Coronary Artery Disease]]): RV infarct occurs in association with IWMI

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]

Central Venous Pressure

  • 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]