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)
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
- Bradyarrhythmia
- Tachyarrythmia
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]])
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

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

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

- 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
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

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)
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]