The Gravedigger’s Guide To The ICU


GI Prophylaxis. 4

Enteral Nutrition.. 4

Pharmacologic.. 4

Decontamination of the GI tract.. 4

Venous Thromboembolism... 6

Risk Factors in Hospitalized Patients. 6

Methods of Thromboprophylaxis. 6

Management of Indwelling Catheters. 8

Scheduled Replacement. 8

Physiological Parameters. 9

Tissue Oxygenation.. 9

Venous O2 Saturation.. 10

Hemorrhage and Hypovolemia.. 12

Crystalloids and Colloids. 16

Calculating Maintenance Fluid.. 16

Acute Heart Failure Syndromes. 18

Systolic Vs. Diastolic Failure. 18

B-Type Natriuretic Peptide. 18

Management Strategies of Compromised Cardiac Output. 19

Mechanical Cardiac Support. 20

Hemodynamic Drug Infusions. 20

Drug Infusion Rates. 21

Receptors. 21

Dobutamine. 21

Dopamine. 22

Nitroglycerin.. 23

Nitroprusside. 24

Norepinephrine. 25

Milrinone. 26

Hypoxemia and Hypercapnia.. 27

Pulmonary Gas Exchange. 27

Quantitative Measures. 27

Hypoxemia.. 30

Hypercapnia.. 31

Oximetry and Capnography.. 32

Oximetry.. 32

Oxygen Inhalation Therapy.. 32

Tolerance of Arterial Hypoxemia.. 32

The End-Point of Oxygen Inhalation.. 33

Methods of Oxygen Inhalation.. 33

The Dark Side of Oxygen.. 34

Acute Respiratory Distress Syndrome.. 34

Severe Airflow Obstruction.. 37

Bedside Monitoring.. 37

Aerosol Drug Therapy.. 38

Acute Management of Asthma.. 38

Acute Management of Chronic Obstructive Pulmonary Disease. 38

Oliguria and Acute Renal Failure.. 40

Oliguria.. 40

Initial Management. 42

Hypertonic and Hypotonic Conditions. 42

Basic Concepts. 42

Hypernatremia.. 43

Hyponatremia.. 47

Antibiotic Use.. 48

Bacteremia.. 48

Treatment of Catheter Related Bacteremia.. 49

Vancomycin Trough.. 49

Hemodynamic Monitoring.. 50

Direct Arterial Blood Pressure Monitoring.. 50

Pulmonary Artery Catheter.. 50

Catheter Insertion.. 50

Troubleshooting.. 51

Cardiovascular Parameters Measurable With A PA Catheter.. 51

Sepsis. 52

Definitions. 52

Multiorgan Dysfunction.. 52

Management of Severe Sepsis and Septic Shock.. 53

Sepsis Management Bundle (within 24 hours of admission) 54

Analgesia.. 56

Sedation.. 56


SOFA.. 58

Neurology.. 60

Gastrointestinal.. 60

Nephrology.. 64

Urine Output. 64

Diuresis. 64

Withdrawal.. 64

Clonidine for Drug Withdrawal. 64

Alcohol Withdrawal (or chronic BZs) 65

Medication Conversion.. 65

Arterial Blood Gas. 65


Common Orders. 67

Medications – IV to PO Conversion.. 68

Medications – Steroids. 68

Equations. 68

Normals. 68

ICU Radiology.. 69

Electrolyte Replacement.. 69

Answer Calls About Respiratory Status (Katie’s Vent Lecture) 70

Respiratory Distress Checklist.. 72

Paperwork.. 72

Admission Note.. 73

Common Orders. 74



GI Prophylaxis

Stress-related mucosal injury occurs when blood flow is inadequate to support the replacement of the mucosal lining, not gastric acidity. Erosions can be demonstrated in 75-100% of ICU patients within 24 hours of admission. Without prophylaxis a clinically apparent hemorrhage will occur in up to 25% and a clinically significant bleed will occur in 1%. Trade off may be an increase in VAP.


Independent risk factors for significant bleed:

  1. Mechanical ventilation for more than 48 hours
  2. Coagulopathy

Preventive Strategies

  1. Preserve gastric blood flow
  2. Enteral Nutrition
  3. Pharmacologic

Enteral Nutrition

Enteral tube feedings can be considered adequate prophylaxis for stress-related gastric hemorrhage unless there is another complicating condition.


Decontamination of the GI tract

Oral Decontamination

The bacterial flora found in critically ill patients changes to include colonization with more virulent pathogens such as Pseudomonas aeruginosa.  This can set up a patient for more severe aspiration pneumonia.


Indications for Oral Decontamination:


Oral Decontaminant

Preparation: have the pharmacy prepare a mixture of 2% gentamicin, 2% colistin, and 2% vancomycin as a paste.

Regimen: Apply paste to the buccal mucosal with a gloved finger every 6 hours until the patient is extubated.



Reduced incidence of pneumonia from 27% to 10% and the mortality rate from 38% to 29%.


Selective Digestive Decontamination




Oral Cavity: As above

GI Tract: A 10 mL solution containing 100 mg polmyxin E, 80 mg tobramycin, and 500 mg amphotericin is given via a NGT q6h

Systemic: Cefuroxime 1.5 grams IV q8hours for four days

Venous Thromboembolism

Risk Factors in Hospitalized Patients

Methods of Thromboprophylaxis

Graded Compression Stockings

These are considered the least effective method of prophylaxis.


Intermittent Pneumatic Compression (SCD)

SCDs are a good choice for patients who are not suitable for anticoagulant prophylaxis due to bleeding risk (such as trauma or post-intracranial surgery.


Low-Dose Unfractionated Heparin

Heparin binds to factor IIa (thrombin) at lower doses than needed to bind to other factors. So low-dose heparin inhibits thrombus formation without producing full anticoagulation.

Can also bind to platelet factor 4 causing development of an antibody causes platelet clumping and thrombocytopenia.


Dosing: LDUH 5000 Units SQ TID


Low-Molecular-Weight Heparin





Enoxaparin (Lovenox) 40 mg SQ Qday (moderate risk) or 30 mg SQ BID (high risk)

Dalteparin (Fragmin) 2500 U SQ Qday (moderate risk) or 5000 U SQ Qday (high risk)





Synthetic anticoagulant that selectively inhibits factor Xa. Its only advantage is that there is no incidence of heparin-induced thrombocytopenia. It is contraindicated in severe renal impairment and patients who weigh less than 50 kg.

Fondaparinux 2.5 mg SQ Qday


Diagnoses of Thromboembolism in the ICU

There is no clinical or laboratory finding in the ICU that will confirm or exclude the diagnosis of pulmonary embolism. A majority of ICU patients (up to 80%) have elevated plasma D-dimer levels). A normal D-dimer may be used to exclude a VTE (NPV 92%). Doppler US does well at detecting DVTs above the knee but can miss 2/3 of DVT below the knees. A negative  Doppler US does not exclude PE.


Treatment of PE

Management of Indwelling Catheters

Scheduled Replacement

Peripheral Venous Catheters

Replace every 3 to 4 days

Central Venous Catheters (not femoral)

Routine replacement is not recommended because it does not reduce infections and increases complications

Central Venous Catheters (femoral)

Replace every 2 days (not prevent  thrombosis, not infection)


Indications for Replacement



Physiological Parameters

Tissue Oxygenation

VO2 is the rate of oxygen delivery

MRO2 is the metabolic requirement for oxygen.

When VO2 < MRO2 (dysoxia) glucose is diverted to anerobic metabolism which results in lactate as a by-product.

Dysoxia can result from:


Calculating VO2

An indwelling pulmonary catheter is needed.



VO2 = Q x 13.4 x Hb x (SaO2 – SvO2)



CaO2= (Hgb x 1.36 x SaO2) + (0.0031 x PaO2)
2= (Hgb x 1.36 x SvO2) + (0.0031 x PvO2)


CaO2: Directly reflects the total number of oxygen molecules in arterial blood (both bound and unbound to hemoglobin)

CvO2: Directly reflects the total number of oxygen molecules in venous blood (both bound and unbound to hemoglobin)

SaO2 = % of arterial hemoglobin saturated with oxygen 
(Normal range: 93-100%)

SvO2 = % of venous hemoglobin saturated with oxygen 
(Normal range: 93-100%)
Hgb = hemoglobin  
Normal range(Adults): Male: 13-18 g/dl  Female: 12-16 g/dl
PaO2= Arterial oxygen partial pressure
(Normal range: 80-100)

PvO2 = Venous oxygen partial pressure


Using VO2

A low VO2 (< 100 mL/min/m2) can be used as evidence of impaired tissue oxygenation. This results in an oxygen debt. The magnitude of oxygen debt (amount and time) correlates with multiorgan failure and death.


Correcting VO2 deficits in patients without sepsis

Augment Cardiac Output

Correct Anemia

Correct Hypoxemia


Correcting VO2 deficits in patients with sepsis

The VO2 is not a true reflection of aerobic metabolism because of the respiratory burst of neutrophils and macrophages. Tissue oxygenation is not impaired in sepsis and therefore therapies designed to improve tissue oxygenation do not seem warranted.


Venous O2 Saturation

A low SvO2 means more oxygen is being extracted by the tissues to compensate for decreased delivery (DO2).

DO2 = Q x [13.4 x Hb x SaO2]

So a decreased DO2 can be caused by decreased cardiac output, anemia or hypoxia.


A drop in SvO2 below 70% indicates that systemic O2 delivery is impaired.

A drop in SvO2 below 50% indicates a global state of hypoxia.


SvO2 is measurement requires a pulmonary artery catheter.


Central Venous O2 Saturation

Measured via a central venous catheter

When averaged over multiple readings the agreement between ScvO2 and SvO2 is within 5%.


Blood Lactate Levels
> 2 mmol/L is abnormal

Lactate and Survivial: There is a delay between dysoxia and an increase in lactate levels.

Clinical Situation


Generalized patients


< 2 mmol/L


>= 10 mmol/L

Do not survive

Circulatory Shock


> 2 mmol/L

60% fatal outcome

> 4 mmol/L

80% fatal outcome

Septic Shock





Other causes of lactate aside from dysoxia


Hemorrhage and Hypovolemia

Total Body Fluid (TBF) is 60% of lean body mass in males and 50% of lean body mass in females.

Most fluid is intercellular and interstitial.


Compensatory Response to Hemorrhage


Progressive Blood Loss

4 categories via American college of surgeons


Clinical Evaluation

Bradycardia may be more common than tachycardia in acute blood loss.

Noninvasive measuring of blood pressure often yields spurious results in low flow states. Intraarterial blood pressure monitoring is recommended.



Supine (not sitting) for one minute. Take BP and pulse. Stand for one minute. Take BP and pulse.

Significant orthostatic change is defined as:



The use of hemoglobin to estimate blood loss is unreliable and inappropriate.

Early changes in hemoglobin represent resuscitation efforts:


Resuscitation Fluid

Expected change in hematocrit

Asanguinous fluid


Whole blood

No change

Packed red cells



Invasive Hemodynamic Monitoring

Central Venous Pressure

Central venous catheters measure cardiac filling pressures (SVC pressure). But these are not an acute representation of blood volume status because of changes in ventricular distensibility. Cardiac filling pressures can provide qualitative information such as <1 mmHg is low and > 15 mm Hg is high.


Systemic O2 Delivery

Cental venous catheters can be used to measure DO2. But in the early stages of hypovolemia VO2 uptake remains unchanged because of increased extraction at the capillaries.

Compensated Hypovolemia

Hypovolemic Shock


Arterial Base Deficit

Base Deficit is gotten from an ABG.

The equation is:


Base Deficit



+2 to –2 mmol/L

Mildly Elevated

-2 to –5 mmol/L

Moderately Elevated

-6 to –14 mmol/L

Severely Elevated

< -15 mmol/L


Correction of the base deficit within house after volume replacement is associated with favorable outcomes.


Arterial Lactate Concentration

Lactate is a marker of impaired tissue oxygenation and a prognostic factor in circulatory shock. Prediction extends to elevated lactate over time.


Volume Resuscitation

Trendelenburg Position

Has not been shown to improve hypovolemia because the central veins are a high capacitance system designed to absorb and limit increased pressure.


Peripheral Vs. Central Venous Cannulation

The rate of volume infusion is determined by the dimension of the vascular catheter, not the size of the vein. Central venous catheters are 6 to 8 inches in length. Peripheral catheters are only 2 inches in length.


Flow Properties of Resuscitation Fluids

Type of Fluid



Fluids with RBCs

Whole blood, packed cells

Increase O2 carrying capacity of blood. Limited by viscosity.

Fluids with large molecules with restricted egress from the vascular space

Plasma, albumin, dextrans, hetastarch

Preferentially increase intravascular volume and cardiac output

Fluids that contain electrolytes and small molecules

Saline, Ringer’s, Normosol

Distribute evenly in extracellular space thereby increasing interstitial volume


Resuscitation Strategies

The end goal of resuscitation is to maintain VO2. By the VO2 equation then was are trying to correct cardiac output and hemoglobin concentration.


Promoting Cardiac Output

Low cardiac output is far more threatening than decreased hemoglobin and so is the first priority.



Blood products

Bad choice for augmenting cardiac output because the viscosity of the effects of erythrocytes may actually decrease cardiac output.


Because plasma volume is only 20% of extracellular fluid, only 20% of the infused volume will remain in the intravascular space.


75-80% of the fluid will remain in the intravascular space in the first couple hours after infusion. This increases preload and decreases afterload (decreased viscosity). But there is a lack of survival benefit over crystalloid resuscitation.


Estimating Resuscitation Volume

  1. Estimate normal blood volume

BV = 66 mL/kg in males or 60 mL/kg in females

  1. Estimate % loss of normal blood

Class I: < 15%

Class II: 15-30%

Class III: 30-40%

Class IV: > 40%

  1. Calculate volume deficit

VD = BV x % blood loss

  1. Determine resuscitation volume

RV = VD x 1.5 (colloid fluid) or VD x 4 (crystalloid)


End-Points of Resuscitation


Correcting Anemia

Anemia should be corrected after volume deficits are replaced and cardiac output is restored. Hemoglobin/hematocrit is a poor indicator for blood transfusion because it will change depending on resuscitation measures/fluids. An O2 extraction of > 50% can be used as a trigger for transfusion.


O2 Extraction (%) = SaO2 – ScvO2

SaO2 is measured with a pulseoximeter.

ScvO2 is measured by a blood sample taken from an indwelling central venous catheter.


Refractory Shock

Prolonged periods of hemorrhagic shock can leave the patient in a state of severe hypotension that is refractory to volume expansion and pressors. Vasopressin at an infusion rate of 1 to 4 mU/kg/min have shown promise at reversing this.


Crystalloids and Colloids

Calculating Maintenance Fluid

100/50/20 per day rule


4/2/1 per hour rule





















Dextrose 5% in Water









Ringer’s Lactate Solution






Lactate 28



Dextrose 5% in Ringer’s Lactate






Lactate 28



Normal Saline (0.9%)









Dextrose 50%









Potassium Chloride











Albumin Solutions

Used in hypoalbuminic states


Hetastarch (Hydroxyethyl starch)

Cleared by kidneys

Oncotic effect lasts only one day

6% hetastarch is equivalent to 5% albumin as a plasma expander and the major difference between the two fluids is that hetastarch is cheaper

Dose related bleeding



Dose related bleeding


Acute Heart Failure Syndromes

Types of heart failure


Causes of heart failure

  1. Supraventricular Arrhythmias
  2. Respiratory failure/PE/Mechanical Ventilation
  3. Complete Heart Block
  4. Ischemia/Infarction/Malignant Arrhythmias
  5. Tamponade, PEEP
  6. Mitral Insufficiency
  7. Aortic Insufficiency
  8. Severe Hypertension/Aortic Dissection


Hemodynamic Changes in Acute Heart Failure

  1. Increase cardiac filling pressures which maintain stroke volume
  2. Decreased stroke volume which is compensated for by an increase in heart rate to maintain cardiac output
  3. Decrease in cardiac output


Cardiac output is impaired only in more advanced stages of heart failure. Therefore a normal cardiac output does not necessarily imply normal cardiac function.


Systolic Vs. Diastolic Failure

EF is decreased in systolic failure and normal in diastolic failure. These can be differentiated by US.


Right Vs. Left Heart Failure

Cardiac US can be used at the bedside. Feature of right heart failure include:

  1. Increased right-ventricular chamber size
  2. Segmental wall motion abnormalities on the right
  3. Paradoxical motion of the interventricular septum


B-Type Natriuretic Peptide



Mean BNP (pg/mL)

Females – no CHF


Age 55-64


Age 75+


Males – no CHF


Age 55-64


Age 75+


Renal Insufficiency


No volume overload


Volume overload


Heart Failure









BNP is usually gotten in the emergency department. It’s role in the ICU is not well defined but it may be used to monitor for the success of treatment regimens.


Management Strategies of Compromised Cardiac Output

Left-Sided (Systolic) Heart Failure

Three important measurements: PCWP, CO, BP

Management is based upon blood pressure.


High Blood Pressure

Profile: High PCWP/Low CO/High BP

Treatment: Vasodilator therapy with nitroprusside or nitroglycerin. If the PCWP remains above 20 mm Hg, add diuretic therapy with furosemide.


Nitroprusside is a vasodilator that augments cardiac output by reducing ventricular afterload. Cyanide toxicity is a problem with continued therapy. Not advised in patients with ischemic heart disease because it can cause “coronary steal syndrome”.


Optimal PCWP is left heart failure is 18-20 mm Hg. Use diuretics only if the PCWP remains above 20 with vasodilator therapy.


Normal Blood Pressure

Profile: High PCWP/Low CO/Normal BP

Treatment: Inodilator therapy with dobutamine or milrinone, or vasodilator therapy with nitroglycerin. If the PCWP does not decrease to < 20 mm Hg, add diuretic therapy with lasix.


Dobutamine and milrinone are inodilators because they have both positive inotropic and vasodilator actions.


Dobutamine is a B-receptor agonist. Blood pressure is usually unaffected but dobutamine may increase BP. Dobutamine can increase myocardial O2 consumption which can be counter productive in ischemic or failing myocardium. Dobutamine can not be used in patients with B-blocker drugs.


Milrinone is a phosphodiesterase inhibitor. Blood pressure is usually unaffected but milrinone may cause hypotension.


Low Blood Pressure (cardiogenic shock)

Profile: High PCWP, Low CO, Low BP

Treatment: Dopamine in vasoconstrictor doses. Mechanical assist devices can be used as a temporary measure in selected cases.


Hemodynamic drugs are notoriously unsuccessfull in cardiogenic shock.


High dose dopamine (>10 microgram/kg/min) acts as a vasopressors and retains some of the positive inotropic actions of low dose (5 to 10 microgram/kg/min).


Diastolic Heart Failure

Because systolic function is normal in diastolic heart failure there is no role for positive inotropic agents.

Diuretic therapy can be counterproductive because it can further impair ventricular filling.


Lusitropic agents (promote ventricular relaxation)


Right Heart Failure


Mechanical Cardiac Support

Hemodynamic Drug Infusions

The 6 Pressor Medications:

  1. Dobutamine
  2. Dopamine
  3. Nitroglycerin
  4. Nitroprusside
  5. Norepinephrine
  6. Milrinone


Initial Choice of Pressors



Left Heart Failure

Primary: Nitroglycerin

Alternatives: Dobutamine, nitropresside

Right Heart Failure


Alternatives: Dobutamine, nitroprusside

Cardiogenic Shock

Primary: Dopamine


Persistent Unstable Angina

Primary: Nitroglycerin


Hypertensive Emergency

Primary: Nitroprusside


Decompensated Heart Failure due to Aortic Stenosis

Primary: Nitroprusside


Septic Shock

Primary: Norepinephrine



Drug Infusion Rates


R = Desired dose are = μg/min

C = Drug concentration in infusate = = μg/mL


Infusion rate = R/C (mL/min)

                     = R/C x 60 (microdrops/min)





Positive inotropic

Positive chronotropic


Peripheral vasodilation


Increased systemic vascular resistance


Cause relaxation of vascular smooth muscle cells (generalized vasodilation)










Adverse Effects





Usual Dose: 3-15 μg/kg/min

Therapy driven by hemodynamic end-points and not be preselected dose rates









Adverse Effects





Usual Dose:

3-10 μg/kg/min to augment cardiac output

10-20 μg/kg/min to increase blood pressure


Dosing is based on ideal body weight (this is not found in other pressors)

Therapy driven by hemodynamic end-points and not be preselected dose rates










Adverse Effects





Usual Dose:

Start at 5-10 μg/min. Increase rate in 5 μg/min increments q5minutes until desired effect is achieved.

Dose requirements should not exceed 400 μg/min. High doses (>350 μg/min) are usually due to drug loss via adsorption or nitrate intolerance.











Adverse Effects





Usual Dose:

Start at 0.2 μg/kg/min and titrate upwards every five minutes to the desired result

Usual range to control hypertension is 2 to 5 μg/kg/min but the dose rate should be kept below 3 μg/kg/min to limit cyanide accumulation. In renal failure limit rate to 1 μg/kg/min.

Max dose is 10 μg/kg/min for only 10 minutes.











Adverse Effects





Usual Dose:

Initial dose may be as low as 1 μg/min and titrated upwards to the desired effect

Effective dose in septic shock is usually 0.2 to 1.3 μg/kg/min (1 to 10 μg/min for a 70kg patient).

Doses as high as 5 μg/kg/min may be required.










Adverse Effects













Do not use vasopressin in patients with heart failure or mesenteric ischemia. In patients with CHF chronic activation of the neuralhormonal axis contributes to progression of disease through an increase in afterload and water retention. Giving vasopressin infusions in patients will cause an increase in systemic vascular resistance and pulmonary capillary wedge pressure which can result in decreased cardiac output. Vasopressin’s affect is most prominent in the capillaries and small arterioles of the splanchnic circulation which can exacerbate mesenteric ischemia.


Hypoxemia and Hypercapnia

Pulmonary Gas Exchange

The adequacy of gas exchange in the lungs is expressed as the V/Q ratio with a perfect match being equal to one.


Dead Space Ventilation (V/Q > 1)

Pattern: PaO2 decreased/PaCO2 increased



Intrapulmonary Shunt (V/Q < 1)

Pattern: PaO2 decreased/PaCO2 normal or decreased



Inhaled oxygen

As the shunt fraction increases, the influence that an increase in fraction concentration of inspired oxygen (FiO2) has on the arterial PO2 becomes less. In conditions with a high shunt fraction (such as ARDS) the FiO2 can be lowered to non-toxic levels (<50%) without compromising arterial oxygenation.


Quantitative Measures

Dead Space Ventilation


Intrapulmonary Shunt Fraction


The A-a PO2 Gradient

A-a gradient =  PAO2 - PaO2
2 (partial pressure of O2 in the artery) --obtained from the arterial blood gases.
PAO2  (partial pressure of O2 in the alveoli)-- obtained from the Alveolar Gas equation.

Alveolar gas equation:
PA02 = PiO2 - (PaCO2 / R)  
     PiO2 = FiO2 (PB - PH2O)
          or  using common values:
                     PA02 = ( FiO2 * (760 - 47)) - (PaCO2 / 0.8)
             *PiO2 = partial pressure of O2 in the central airways
             *FiO2 (fraction of inspired oxygen)   FiO2 on room air = 0.21
             *PaCO2 (value from your ABG).
             *PB = barometric pressure (760 mmHg at sea level)
                       PB = PN2 + PO2  + PCO2  +PH2O
             *PH2O = Water vapor pressure (47 mm Hg at 37 degrees celcius)
             *R = Respiratory quotient = VCO2 / VO2 = 0.8 (usual)
                      (ratio of carbon dioxide production to oxygen consumption.)

Estimating A-a gradient:
        Normal A-a gradient = (Age+10) / 4
         A-a increases 5 to 7 mmHg for every 10% increase in FiO2


The a/A PO2 Ratio

Equation is independent of the FiO2


a/A PO2 = 1 – (A-a PO2)/PaO2


The PaO2/FiO2

An indirect estimate of shunt fraction. Not good for oxygen delivered via nasal prongs or face mask due to FiO2 variability.



Qs/Qt (shunt fraction)

< 200

> 20%

> 200

< 20%


Blood Gas Variability

ABGs can vary spontaneously without a change in patient condition. PO2 may vary by as much as 36 mm Hg and PCO2 may vary by as much as 12 mm Hg.



Sources of hypoxemia:


A-a PO2





V/Q mismatch



DO2/VO2 imbalance





There is a decrease in the volume of air inhaled and exhaled each minute. There is no V/Q imbalance so the A-a PO2 gradient is not elevated.



V/Q Abnormality



DO2/VO2 Imbalance

As the impairment in alveolar oxygen exchange increases there is an increased contribution of the mixed venous blood PO2 to the arterial PO2.


Diagnostic Evaluation


Spurious Hypoxemia

Can occur with hematologic problems such as marked leukocytosis (>100,000) or thrombocytosis (>1,000,000).




Oximetry and Capnography


Lambert-Beer Law: The absorption of light as it passes through a medium is proportional to the concentration of the substance that absorbs the light and the length of the path that the light travels.


In the red spectrum light (660 nm) deoxygenated hemoglobin absorbs light better. In the infrared region of light (940 nm) oxygenated hemoglobin absorbs light better. Bedside oximeters use these two fractions to estimate the percent oxygenated hemoglobin.


Early oximeters were placed on the ear and could not tell the difference between blood in an artery and a vein. Modern oximeters use a photodetector which amplifies only light of alternating intensity (arterial blood).


Accuracy: Less than 3% difference from actual SaO2 at clinically acceptable levels of arterial oxygenation (SaO2 > 70%).


Special Conditions

Pulse oximetry is unreliable for detection of hypoxemia in carbon monoxide intoxication.

Pulse oximetry overestimates the SaO2 in states of methemoglobinemia.

Pulse oximetry is reliable in its detection of pulsatile blood flow down to blood pressures as low as 30 mm Hg

In cases where there is severely reduced peripheral blood flow to the fingers, special oximeters are available for placement on the forehead.

Pulse oximetry is accurate in anemia to hemoglobin levels as low as 2 to 3 g/dL

Methylene blue (used to treat methemoglobinemia) can produce a 65% decrease in detected SaO2


Venous Oximetry



Oxygen Inhalation Therapy

Tolerance of Arterial Hypoxemia

Standard indications for supplemental oxygen:

But…in the resting patient, even the most severe clinical hypoxemia due to pulmonary insufficiency does not lead to generalized tissue anaerobiasis (as measured by lactate).


The End-Point of Oxygen Inhalation

Although supplementary oxygen inhalation may increase PaO2 or SaO2 it may not be used as evidence of increased tissue oxygen delivery. Oxygen has a tendency to reduce systemic blood flow. It is a vasoconstrictor in all vascular beds except the in the pulmonary circulation. In the absence of hypoxemia it can also reduce cardiac output because it is a negative inotrope.

Methods of Oxygen Inhalation

Oxygen delivery methods are classified as low-flow or high-flow systems:


Oxygen Inhalation Systems

Nasal Prongs

The nasopharynx acts as an oxygen reservoir. As minute ventilation increases the FiO2 rapidly declines because of the small reservoir.


Low-Flow Oxygen Masks

Face masks add 100 to 200 mL to the oxygen reservoir. These can deliver oxygen at 5 to 10 L/min. The minimum flow rate is 5 L/min because this is the minimum need to clear exhaled gas from the mask.


Masks with Reservoir Bags

A reservoir bag adds a reservoir capacity of 600 to 1000 mL to a standard face mask. There are partial rebreather systems which allow some of the patients exhaled air to mix into the reservoir bag and nonrebreather systems that prevent this. Nonrebreather devices allow the inhalation of pure oxygen.


High-Flow Oxygen Masks

Oxygen is delivered to the mask at low flow rates but there is a narrowed orifice at the inlet of the mask that creates a high-velocity stream of gas that drags room air into the mask. At any given FiO2 the proportion of inhaled gas remains fixed regardless of changes in respiratory rate which is an advantage in patients with chronic hypercapnia (because an inadvertent increase in FiO2 can lead to further CO2 retention).


Low-Flow Oxygen Inhalation Systems


Reservoir Capacity

Oxygen Flow (L/min)

Approximate FiO2

Nasal cannula

50 mL























Oxygen face mask

150-250 mL




750-1250 mL



Partial rebreather









The Dark Side of Oxygen

FiO2 above 0.60 for longer than 48 hours constitutes a toxic exposure to oxygen.


Acute Respiratory Distress Syndrome


ARDS is an inflammatory process in which systemic activation of circulating neutrophils cause them to deposit bilaterally in the vascular endothelium. There they release cytoplasmic granules which damage the endothelium and leads to a leaky-capillary type of exudation into the lung parenchyma. Neutrophils and proteinaceous material gain access to the lung parenchyma and fill the alveolar spaces. The damage caused by this can perpetuate the cycle.

Fibrin also is deposited in the lungs due to the procoagulant state of the injuryed lung parenchyma.


Predisposing Conditions

High risk conditions are:


Clinical Features

Onset is usually as tachypnea and progressive hypoxemia that is refractory to supplemental oxygen.


Diagnostic Criteria for ALI and ARDS

Acute Onset

Presence of a predisposing condition

Bilateral infiltrates on frontal CXR

PaO2/FiO2 < 200 mm Hg for ARDS, and < 200 mm Hg for ALI

Pulmonary artery occlusion pressure <= 18 mm Hg or no clinical evidence of left atrial hypertension


Differential Diagnosis

Features Shared by ARDS & Other Causes of Acute Respiratory Failure



Severe PNA


Cardiogenic Lung Edema

Acute onset

Fever, Leukocytosis

If acute MI

Bilateral infiltrates


PaO2/FiO2 < 200 mm Hg


PAOP <= 18 mm Hg



Bronchoalveolar Lavage

The most reliable method for confirming or excluding the diagnosis of ARDS is bronchoalveolar lavage. The lavage fluid is analyzed for neutrophil density and protein concentration. Neturophils are usually less than 5% of a BAL. In ARDS they may make up as many as 80% of the recovered cells.


Lights criteria may also be used to differentiate the exudative fluid of ARDS from the transudative fluid of cardiogenic edema.


Protein (lavage/serum) < 0.5 = Hydrostatic pressure

Protein (lavage/serum) > 0.7 = Lung inflammation


Management of ARDS

There is not a homogenous pattern of lung infiltration in ARDS. Instead it is confined to dependant lung regions. The amount of functional lung volume is reduced in ARDS and so large inflation volumes lead to ventilator-induced lung injury .


The only therapeutic manipulation that has proven effective in improving survival in ARDS is the use of low tidal volume mechanical ventilation.


Protocol for Low Volume Ventilation in ARDS


Goals: TV = 6 ml/kg (IBW), Ppl < 30 cm H2O, pH = 7.30 – 7.45


  1. First Stage
    1. Calculate patient’s predicted body weight (PBW)
    2. Set initial tidal volume to 8 ml/kg PBW
    3. Add PEEP at 5-7 cm H2O
    4. Reduced TV by 1 mL/kg every 2 hours until TV = 6 ml/kg PBW
  2. Second Stage
    1. When TV down to 6 ml/kg, measure plateau pressure (Ppl)

                                                               i.      Target Ppl < 30 cm H2O

                                                             ii.      If Ppl > 30 cm H2O decrease TV in 1 ml/kg steps until Ppl drops below 30 cm H2O or TV down to 4 mL/kg

  1. Third Stage
    1. Monitor arterial blood gas for respiratory acidosis

                                                               i.      Target pH = 7.3 – 7.45

                                                             ii.      If pH 7.15 to 7.30, increase RR until pH > 7.30 or RR = 35 bpm

                                                            iii.      If pH < 7.15, increase RR to 35 bpm. If pH still < 7.15, increase TV at 1 mL/kg increments until pH > 7.15


Calculating Predicted Body Weight (PBW)

Males: PBW = 50 + [2.3 x (height in inches – 60)]

Females: PBW = 45.5 + [2.3 x (height in inches – 60)]


Permissive Hypercapnia

Low tidal volume ventilation comes at the cost of a reduction in CO2 elimination. Increased CO2 leads to hypercapnia and respiratory acidosis. Hypercapnia to arterial PCO2 levels of 60-70 mm Hg and arterial pH levels of 7.2 to 7.25 are safe for most patients. The risks should be weighed against the benefits.

Positive End-Expiratory Pressure

Low levels of PEEP help keep open alveoli. This reduces shear stress on them from constant opening and closing and also may reduce the FiO2 requirement.


FiO2:PEEP Combinations for Promoting Arterial Oxygenation in ARDS

Goals: PaO2 = 55-80 mm Hg or SpO2 = 88-95%







































PEEP can decrease cardiac output due to decreased venous return.


Fluid Management


Promoting Oxygen Transport

The goal is to maintain oxygen delivery to vital organ tissues by:



Severe Airflow Obstruction

Bedside Monitoring

Clinical exam is notoriously inaccurate in assessing the presence and severity of airflow obstruction.



The standard index of airflow obstruction is the FEV1/FVC. The FEV1 is the forced expiratory volume in one second and the FVC is the forced vital capacity. A ration of less than 0.7 indicated airflow obstruction. This is a difficult test at the badside.


Peak Expiratory Flow Rate (PEFR)

The PEFR is the greatest flow velocity that can be obtained during a forced exhalation starting with lungs fully inflated. This is measured with a peak flow meter. This is effort dependent. The greatest flow velocity is a surrogate for the elastic recoil of the lungs and the caliber of the airway (both of which are greatest very early in exhalation).


A PEFR reference table is needed to interpret the PEFR of individual patients. But there are some general statements.


Applications of Peak Expiratory Flow Rate

Severity of Airway Obstruction

PEFR (% Predicted)



Mild obstruction


Moderate obstruction


Severe obstruction


Respiratory failure

Bronchodilator Responsiveness

PEFR (% increase)



Favorable response


Equivocal response


Poor response


Assessing the Benefits of Bronchodilators

Inhaled bronchodilators are routinely used for COPD patients in the hospital although they may confer little benefit. The benefit for an individual patient can be assessed by measuring the PEFR before and after a treatment.

Bronchodilators are also routinely given to ventilator patients. One can assess the benefit of these on a ventilator patient by watching for a fall in the Peak Inspiratory Pressure with bronchodilator therapy.

Aerosol Drug Therapy

Nebulizer versus MDI

There is an equivalent response after two doses with either method. MDIs cost much less in the hospital setting and so are preferred.


Aerosols in Ventilator Patients

Aerosol deposition in the lungs of mechanical ventilated patients is reduced and so doses may need to be increased.


Acute Management of Asthma

Acute Management of Chronic Obstructive Pulmonary Disease

COPD is a condition of chronic obstruction that is defined apart from asthma because of it’s limited responsiveness to bronchodilators.


Treatment consists of four pathways: bronchodilators, steroids, antibiotics and respiratory support.


Antibiotic Selection for Acute Exacerbation of COPD Based on Risk

Risk Assessment:

  • Is the FEV1 less than 50% predicted?
  • Does the patient have cardiac disease or other significant comorbidities?
  • Has the patient had 3 or more exacerbations in the previous 12 months?

If the patient answers “yes” to at least one of these, they are considered high-risk

Antibiotic Selection

  • High Risk: Amoxicillin-clavulanate or a newer fluoroquinolone (gatifloxicin, levofloxacin, or moxifloxacin)
  • Low Risk: Doxycycline, a 2nd generation cephalosporin (e.g. cefuroxime) or a newer macrolide (azithromycin or clarithromycin)


Oliguria and Acute Renal Failure


The Multiple Definitions of Oliguria

  • Less than 0.5 mL/kg/hr (about 35 mL/hr in a 70 kg patient)
  • Less than 16.6 mL/hr
  • Less than 400 mL/day

Causes of Oliguria

Evaluation of Oliguria

Central Venous Catheters
Arterial Line

In ventilator dependent patients, a decrease in blood pressure shortly after each lung inflation can be used as evidence of inadequate cardiac filling.


Urine Microscopy



Epithelial cells and epithelial cell casts


White cell casts

Interstitial nephritis

Pigmented casts



Spot Urine Sodium

Decreased renal perfusion => increased sodium reabsorption => fluid retention

Intrinsic renal disease => decreased sodium reabsorption


Fractional Excretion of Sodium

The FEna is normally < 1%. In the setting of oliguria:


Serum Creatinine Concentration

A change in serum creatinine concentration can be used to identify patients with renal injury and renal failure. The serum creatinine can also be used to calculate the creatinine clearance using the Cockcroft and Gault equation.

CrCl = [(140 - age) x IBW] / (Scr x 72)       (x 0.85 for females)

Note: if the ABW (actual body weight) is less than the IBW use the actual body weight for calculating the CRCL. If the patient is  >65yo and creatinine<1.0,  use 1 to calculate the creatinine clearance.


Estimating Ideal Body Weight:
Males: IBW = 50 kg + 2.3 kg for each inch over 5 feet.
Females: IBW = 45.5 kg + 2.3 kg for each inch over 5 feet.


Initial Management

Fluid challenges of 500 mL to 1,000 mL crystalloid fluid infused over 30 minutes.


Specific Renal Disorders

Inflammatory Renal Injury

Contrast-Induced Nephropathy

Acute Interstitial Nephritis

Myoglobinuric Renal Failure

Renal Replacement Therapy


Hypertonic and Hypotonic Conditions

Basic Concepts

Osmotic Activity

Osmolarity is the osmotic activity per volume of solution (solutes plus water). Osmolality is the osmotic activity per volume of water. These terms can be used interchangeably to describe the osmotic activity in body fluids because the volume of water in body fluids is so much greater than solutes. Higher osmolality means higher solute concentration.



Tonicity is only used when comparing two solutions. It is essentially the relative or effective osmotic activity. The solution with a high osmotic activity (draws water in) is called hypertonic. The solution with the lower osmotic activity (losses water) is called hypotonic.

If a membrane separating two fluids is permeable to both water and the solute and a solute is added to one compartment, it is the solute that will equilibrate fully across the membrane. The solute increases the osmolality of both fluids equally and there is no net movement of water. This creates a hyperosmotic condition but not a hyperosmotic condition. This is what happens with an increase in urea (azotemia).


Plasma Osmolality

Plasma osmolality is determined in the laboratory but measuring the freezing point. It can also be calculated as:


Plasma Osmolality =  (2 x Na) + (Glucose/18) + (BUN/2.8)


A normal plasma osmolality is 290 mOsm/kg H2O. Sodium is multiplied by two to account for chloride. The division factors for glucose and BUN are conversion factors.


Osmolal Gap

The osmolal gap is the difference between the calculated and measure plasma osmolality. It can be used as a screening test for toxins in the extracellular fluid or


Plasma Tonicity

Since urea passes freely across cell membranes it is not included when calculating plasma tonicity.

Plasma Tonicity =  (2 x Na) + (Glucose/18)


Hypernatremia results from either:


It is important to first determine the extracellular volume status:

Treatment for each of these states is different.

Volume Status



Replace sodium deficit quickly and replace free water deficit slowly


Replace free water deficit slowly


Induce sodium loss with diuresis and replace urine volume loss with fluids that are hypotonic to the urine.


Hypovolemic Hypernatremia

Most body fluids contain more free water than sodium and so their loss will cause both hypovolemia and hypernatremia.


Sodium Concentration in Body Fluids




< 10 (varies according to intake



Gastric Secretions




Furosemide diuresis


Pancreatic secretions


Small bowel secretions



Hypovolemia is the most immediate threat in this state, although it is not as severe as when whole blood is lost because the resultant hypertonicity draws water out of cells to maintain extracellular fluid status.

The most fear complication of the hypertonicity state is a metabolic encephalopathy due to cellular dehydration. This must be corrected slowly because neurons metabolically adjust to their hypotonic state by producing solutes to maintain tonicity (idiogenic osmoles). If the hypernatremia is corrected too fast the neuronal cells may swell and burst.


Volume Replacement

Replace volume to maintain cardiac output and urine output. Colloids may be more effective than crystalloids.


Free Water Replacement
  1. Calculate the Normal TBW


Normal TBW is calculated as 10% less than usual in hypernatremia. Therefore in men it is 50% of lean body weight and in women it is 40% of lean body weight.


  1. Calculate the Current TBW


Current TBW = Normal TBW x (140/Current Pna)


  1. Calculate the TBW Deficit


TBW Deficit = Normal TBW – Current TBW


  1. Calculate the Volume Needed to Correct the Fluid Deficit


Replacement Volume (L) = TBW x (1/1-X)


X is the ratio of sodium concentration in chosen fluid to the sodium concentration in isotonic fluid (154 mEq/L). If NS is given then X = 1. If ½ NS is given then X = 0.5.


  1. Track Daily Progress

Due to the risk of cerebral edema, free water should be replaced slowly so that serum sodium decreases no faster than 0.5 mEq/L per hour


Hypertonic Syndromes

Diabetes Insipidus

The underlying problem in DI is a failure related to antidiuretic hormone (ADH), a hormone secreted by the posterior pituitary that  promotes water reabsorption in the distal tubule.


Central DI

Central DI is a failure of the posterior pituitary to secrete ADH.

Common causes are:

·        Traumatic brain injury

·        Anoxic encephalopathy

·        Meningitis

·        Brain death

The onset of central DI is heralded by polyuria that is usually evident within 24 hours of the inciting event.


Nephrogenic DI

Nephrogenic DI is caused by defective end-organ responsiveness to ADH.

Causes of nephrogenic DI are:

·        Amphotericin

·        Dopamine

·        Lithium

·        Radiocontrast dyes

·        Hypokalemia

·        Aminoglycosides

·        ATN – polyuric phase

The defect in the kidneys ability to concentrate urine is not so bad as in central DI.



·        Urine Osmolarity

o       Central DI: < 200 mOsm/L

o       Nephrogenic DI: between 200 and 500 mOsm/L

·        Fluid Restriction

o       Failure of urine osmolarity to increase more than 30 mOsm/L in the first few hours of complete fluid restriction.

·        Response to Vasopressin 5 Units IV

o       Central DI: the urine osmolarity will increase by at least 50% nearly immediately

o       Nephrogenic DI: the urine osmolarity will remain unchanged



·        Calculate free water losses and begin slow replacement

·        If central DI, give vasopressin 2-5 Units SQ q4-6hours

·        Monitor carefully during vasopressin therapy for water intoxication and hyponatremia as central DI begins to resolve


Non-Ketotic Hyperglycemia

Non-ketotic hyperglycemia occurs when a state of hyperglycemia develops in patients that have enough endogenous insulin to prevent ketosis.


Clinical manifestations

The plasma glucose is usually above 1000 mg/dL whereas in ketoacidosis the plasma glucose is usually below 800 mg/dL. Water loss occurs because of osmotic diuresis and plasma tonicity may rise above 330 mOsm/kg H2O. Encephalopathy may procede to seizures and focal neurological deficits.



Rapid correction with colloid fluids may be necessary.

Free water deficits are estimates and corrected as in hypovolemic hypernatremia. The only difference is that sodium value needs to be corrected. For every 100 mg/dL increment in the plasma glucose the plasma sodium should fall by 1.6 to 2 mEq/L. Restoration of brain cell volume can occur rapidly and therefore the free water replacement should be particularly judicious.


Insulin Therapy

Insulin therapy drives both glucose and water into cells and so can aggrevate hypovolemia. Hold insulin until the vascular volume is restored.

Hypervolemic Hypernatremia






Extreme elevations in plasma lipids or protein can increase the volume of the nonaqueous/nonsodium containing phase of plasma which will falsely lower the sodium.


Hypotonic Hyponatremia

Like hypernatremia the first step in managing hyponatremia is to assess extracellular volume.



Hypovolemic Hyponatremia

This is causes by loss of body fluid containing sodium and replacement with fluid which does not contain sodium.  A urine sodium can differentiate whether the losses are a renal or extrarenal origin as shown above.


Isovolemic Hyponatremia


Hypervolemic Hyponatremia

This is caused by a gain of both sodium and water with water gain exceeding sodium. A urine sodium can help differentiate the causes. Diuretic use can complicate the differentiation.


Management Strategies

The rate of rise in plasma sodium should not exceed 0.5 mEq/L per hour and the final plasma sodium concentration should not exceed 130 mEq/L.


Volume Status



Infuse hypertonic saline (3% NaCl) in symptomatic patients and isotonic saline in asymptomatic patients

Normal ECV

Combine furosemide diuresis with infusion of hypertonic saline in symptomatic patients or isotonic saline in asymptomatic patients.

High ECV

Use furosemide-induced diuresis in asymptomatic patients. In symptomatic patients, combine furosemide diuresis with judicious use of hypertonic saline.


Sodium Replacement

When corrective therapy requires the infusion of isotonic saline or hypertonic saline, a sodium deficit should be calculated to guide therapy.


Sodium deficit (mEq) = Normal TBW x (130 – Current Pna)


To get the mL of replacement fluid needed, divide the deficit by 513 mEq (if using 3% sodium chloride or 154 mEq for isotonic saline. This amount will be in liters.


Then find the amount of time over which the deficit should be replaced (maximum rise of 0.5 mEq/L per hour).


Then order to give the replacement fluid needed over the time required.



Antibiotic Use


Usually catheter related



ICU Frequency

Coagulase-negative staph (epidermitis)




Gram Negative Aerobic Bacilli

  • Pseudomonas
  • Klebsiella
  • E coli


Staph aureus







Treatment of Catheter Related Bacteremia

Clinical Condition

Initial Management

Isolated fever

Leave catheter in place and draw paired quantitative blood cultures

Consider Rx with vancomycin pending culture results

Severe Sepsis or Septic Shock

Remove catheter

Start Rx with Vancomycin + ceftazidime (or cefepime for pseudomonas)


Remove catheter

Start Rx with Vancomycin + imipenem

Prosthetic valve

Remove catheter

Start Rx with Vancomycin + aminoglycoside


Follow Culture Results and change ABX appropriately.


Length of Treatment:


Commonly Use

Vancomycin Trough

Consider loading doses in obese patients:

• Obese = actual body weight > 120% IBW

• Give 1500 mg loading dose for obese patients weighing 85 – 109 kg

• Give 2000 mg loading dose for obese patients weighing > 110 kg


Initial maintenance dose:

Estimated CrCl (ml/min)

Initial dosing regimen

Continuous Renal Replacement


1000mg IV q 24 h

< 20 and/or intermittent hemodialysis

1000 mg dose IV q 72 h


1000 mg IV q 48 h


1500 mg IV q 48 h


750 mg IV q 24 h


1000 mg IV q 24 h


1000 mg IV q 12 h

100-120, age > 65

1000 mg IV q12 h

100-120, age < 65

1250 mg IV q 12 h

120 and/or hypermetabolic state**

1000 mg IV q 8 h

** Hypermetabolic states include trauma and burn patients

Trough Serum Concentration1

Dose Adjustment Recommended



<3.5 mg/L

Shorten dose interval to next standard interval:

If Q48H then Q24H, If Q24H then Q12H

If Q12H then Q8H, If Q8H then Q6H

Draw trough level thirty (30) minutes prior to 3rd dose of new dosing regimen

3.5-4.9 mg/L

Increase dose by 250 mg to 500 mg at same time interval. If improvement in renal function3, consider shortening interval.

Draw trough level approximately 30 minutes prior to 3rd dose of new dosing regimen

5-15 mg/L

No change in therapy4

No further trough levels to be drawn unless:

• Duration of therapy is >7 days; If therapy >7 days, check trough level every 5 to 7 days

• Patient status declines

•Serum creatinine increases >0.5 mg/dL from baseline


15.1-19.9 mg/L

Decrease dose by 250 mg at same time interval

Draw trough level approximately 30 minutes prior to 3rd dose of new dose regimen therapy

≥ 20 mg/L and

Dose ≥ 1000 mg

Decrease dose by 500 mg at same time interval


If decline in renal function3, hold dose(s) and check another level in 12-24 hours. When trough is therapeutic, restart at lower dose and/or extend interval, based on patient-specific clearance.

Draw trough level approximately 30 minutes prior to 3rd dose of new dose regimen therapy

≥ 20 mg/L and

Dose < 1000 mg

Extend dose interval to next standard interval:

If Q6 then Q8

If Q8 then Q12

If Q12 then Q24

If Q24 then Q48


If decline in renal function, hold dose and check another level in 12-24 hours. When through is therapeutic restart at appropriate dosing for function.

Draw trough level approximately 30 minutes prior to 3rd dose of new dose regimen therapy


Hemodynamic Monitoring

Direct Arterial Blood Pressure Monitoring


Pulmonary Artery Catheter


Catheter Insertion




Catheter will not advance into the right ventricle

Can occur with tricuspid regurgitation or right heart failure.

Replace the air in the catheter with saline and place patient on left side. Remove saline and replace with air once right ventricle is entered.

Catheter will not advance into the pulmonary artery

Catheter may be coiled. This may be a problem in a patient with pulmonary hypertension. Try pulling back to the SVC and then re-advancing very slowly.


Atrial and ventricular arrhythmias are common and usually benign. Complete heart block is not benign and the catheter should be immediately withdrawn. Transcutaneous pacing may be necessary.

Unable to obtain wedge pressure

Occurs in 25% of PA catheter placements. Use pulmonary artery diastolic pressure as the pulmonary wedge pressure (should be the same unless there is pulmonary hypertension).


Cardiovascular Parameters Measurable With A PA Catheter


Measuring Wedge Pressure

The catheter most likely will migrate into a smaller artery so inflate the balloon slowly until a wedge tracing is obtained.



Systemic Inflammatory Response Syndrome (SIRS)

The diagnosis requires at least two of the following:

  1. Temperature > 38°C or < 36°C
  2. Heart Rate > 90 beats/min
  3. Respiratory Rate > 20 breaths/min or Arterial PCO2 < 32 mm Hg
  4. WBC count > 12,000/mm3 or < 4000/mm3 or > 10% immature band forms


Sepsis is SIRS that is the result of an infection.

Severe Sepsis

Severe sepsis is sepsis that is accompanied by dysfunction of one or more organ system.

Septic Shock

Septic shock is severe sepsis that is accompanied by hypotension that is refractory to volume infusion.

Multiorgan Dysfunction

Clinical Syndromes most commonly associated with MOD


Management of Severe Sepsis and Septic Shock

Early Goal-Directed Therapy/Sepsis Resuscitation Bundle

  1. Serum lactate measured
  2. Blood cultures obtained before antibiotic administration
  3. Improved time to broad-spectrum antibiotics
  4. In the event of hypotension or lactate >4 mmol/L (36 mg/dL)
  5. In the event of persistent hypotension despite fluid resuscitation or lactate > 4 mmol/L


These guidelines were made by consensus best judgment sometimes without great supporting evidence.

Sepsis Management Bundle (within 24 hours of admission)

  1. Administer low-dose steroids
  2. Administer drotrecogin alfa (activated)
  3. Maintain adequate glycemic control
  4. Prevent excessive inspiratory plateau pressures

Low dose steroids

Prolong time to death instead of increasing survival.

Give Hydrocortisone 200-300 mg IV daily in 2 or 3 divided doses for 7 days.

Drotrecogin Alfa

Recombinant activated protein C [rhAPC] for patients at high risk of death:

PROWESS study showed significant reduction in 28 day all-cause mortality

Maintain Glycemic Control

Following stabilization, blood glucose should be maintained at 80-110 mg/dL via continuous insulin infusion and frequent monitoring.

Reduces newly-acquired kidney injury, promotes accelerated weaning from ventilation and accelerated discharge from ICU.

Prevent Excessive Inspiratory Plateau Pressures

Keep inspiratory plateau pressure at < 30 cm H2O to prevent lung injury and further inflammation.



Consider patient baseline tolerance.


Morphine IV

Intermittent Dosing: 2mg, then titrate up 1 mg to 2 mg every few hours

Continuous Dosing: 1mg/hour

Adjust dosing for renal insufficiency


Morphine Intrathecal

Dose: 0.25-0.5 mg

Peaks twice. The first is soon after administration and within the site of injection. The second peak occurs 12 to 24 hours later and is supraspinal as the drug circulates rostrally.

SideEffects: Fewer and less respiratory depression. But respiratory depression may be delayed by up to 24 hours and so patients should be monitored.

Notes: If a patient has been given intrathecal morphine within the last 24 hours do not give them PCA pump. Give them short-acting narcotics and watch for second peak.


Hydromorphone (Dilaudid)

Intermittent Dosing: 0.2 to 0.6 mg with repeated doses every 2 to 3 hours

Continuous Dosing: Bolus dose and then 0.5 to 1.0 mg/hour

Potency: More potent than morphine

Adjust dosing for hepatic failure


Fentanyl (Duragesic)


Potency: 100 times more potent than morphine

Intermittent Dosing: 25 to 75 mcg/hour

Continuous Dosing (more effective): bolus dose and then 25-50 mcg/hour

Side Effects: Accumulates in adipose tissue if administered for longer than 5 days and so may have prolonged affects.

Adjust dosing for hepatic failure



Diprivan (propofol) can cause pancreatitis, excess TGs

Versed vs. ativan (ativan’s long half life means you can’t extubate after stopping until the next day)

Sedation scale, daily discontinuation decreases length of stay


Lorazepam (ativan) can cause hyperosmolar metabolic acidosis in ICU patients on a continuous infusion because of the carrier molecule propylene glycol. Propylene glycol toxicity is increased by renal or liver failure or coadministration of drugs that also use it as a carrier (Phenobarbital, phenytoin, bactrim, etomidate, nitroglycerin).


Dosing and Half-life of Action of Selected Sedative


Onset after IV dose

Half-life or parent compound

Intermittent IV dose (quick 70 kg dose)

Infusion Dose Range (quick 70 kg dose)

Lorazepam (Ativan)

5-20 min

8-15 hr

0.02-0.06 mg/kg q2-6 hr (1.4-4.2 mg)

0.01-0.1 mg/kg/hr (0.7-7 mg)

Diazepam (Valium)

2-5 min

20-120 hr

0.03-0.1 mg/kg q0.5-6 hr (2.1-7 mg)


Midazolam (Versed)

2-5 min

3-11 hr

0.02-0.08 mg/kg q0.2-2 hr (1.4-5.6 mg)

0.04-0.2 g/kg/hr (2.8-14 mg)

Propofol (Diprivan)

1-2 min

26-32 hr


5-80 μg/kg/hr (350-5600 μg)

Haloperidol (Haldol)

3-20 min

18-54 hr

0.03-0.15 mg/kg q0.5-6 hr (2.1-10.5 mg)

0.04-0.15 mg/kg/hr (2.8-10.5 mg)

Predicting Prognosis


What is the patient’s Apache II score on admission (take worse values of first 24 hours)




What is the patient’s SOFA score trend?


SOFA score and mortality

Initial Score

Mortality Rate

Highest Score

Mortality Rate

































Is the patient sedated?

What is the state of consciousness?



What size are pupils?

Are pupils reactive?

Small reactive pupils may be due to a toxic-metabolic disturbance. Very small pupils (pinpoint) that react to naloxone are characteristic of narcotic overdose. Pinpoint pupils that are poorly reactive are characteristic of pontine dysfunction. Lesions rostral or caudal to the midbrain may disrupt descending sympathetics and produce small pupils. Bilateral, widely dilated, fixed pupils are due to sympathetic overactivity from an endogenous cause (seizures or severe anoxic ischemia) or exogenous catecholamines (dopamine or norepinephrine) or atropine-like drugs.



Upper GI Bleed

Mortality is approximately 10%, usually not from blood loss but from decompensation of other underlying conditions.



  1. PUD (50%)
    1. Idiopathic
    2. Asa, NSAID
    3. Infectious (h. pylori, CMV, HSV)
  2. Stress-related
  3. Zollinger-Ellison
  4. Esophagitis
    1. Peptic
    2. Infectious (h. pylori, CMV, HSV)
    3. Meds (NSAID, ASA, alendronate)



  1. Dieulafoy lesion
  2. Idiopathic angiomas
  3. Osler-Weber-Rendu
  4. Watermelon stomach
  5. Radiation-induced telangiectasia
  6. Blue rubber bleb nevus syndrome


Portal HTN

  1. Esophageal varices
  2. Gastric varices
  3. Portal hypertensive gastropathy



  1. Benign (lei, polyp, lipoma)
  2. Malignant



  1. Mallory-Weiss tear
  2. NGT
  3. Foreign body ingestion



  1. Hemobilia
  2. Hemosuccus pancreatitis






Choosing placement

Determine amount of blood lost:


Diagnostic Workup


Predictors and Risk Stratification

Independent Predictors of Death and Rebleeding

  1. Patient Characteristics
    1. Hemodynamic instability
    2. Older age
    3. Comorbidities
  2. Amount of Bleeding
    1. Continued hematemesis
    2. Hematochezia
    3. Gastric Lavage with BRB that doesn’t clear
    4. Hemorrhagic Shock
    5. High Transfusion Requirement (>2U)
    6. Hct drop of more than 6%




  1. Close monitoring in ICU if bleeding is significant
  2. Place a large nasogastric tube
  3. Large bore IV access
    1. At least two 14- or 16-gauage peripheral IVs
    2. Or a 12F double lumen catheter or a 9 Fr introducer
  4. Volume resuscitation for hemodynamic stability
  5. Transfuse PRBC to maintain hemoglobin
    1. >7 g/dL in healthy, young
    2. >10 g/dL in elderly, comorbid
  6. Correct coagulopathy
    1. Platelets to >50,000
    2. FFP and vitamin K for PT within 2 seconds of normal
    3. Recombinant factor VII can rapidly correct coagulopathy of severe liver failure
  7. Consult gastroenterology and surgery if bleeding severe



  1. Acid suppression
  2. Splanchnic vasoconstrictors for variceal bleeding
    1. Ocreotide
    2. Vasopressin analogues
  3. Antibiotics (fluoroquinolones) for variceal bleeding
  4. Upper GI endoscopy
    1. Early for high risk patients
    2. Later for low risk patients
  5. Elective intubation for patients with AMS or who may aspirate during EGD
  6. Angiography (as indicated)
  7. Surgery


Pharmacologically Treatment

Proton Pump Inhibitors

PPIs have been shown to decrease the rate of rebleed

Protonix: 80mg IV bolus, followed by 8mg/hr infusion continued for 48-72 hours and then switched to BID dosing if no rebleed


Splanchnic Vasoconstrictors

Octreotide: 50 microgram bolus, followed by an infusion of 50 microgram/hour for 5 days



For cirrhotic patients, give prior to EGD



Avoid splanchnic dilator such as dopamine



Findings that predict risk of rebleeding


Prevalence (%)

Risk of rebleed (%)

Clean ulcer base



Flat spot



Oozing without visible vessel



Adherent clot



Nonbleeding visible vessel



Active arterial bleeding





Life-threatening hemorrhage refractory to pharmacologic and endoscopic intervention


Urine Output

Normal output is 800 to 1500 ml urine/day

Minimum is 500-600 ml/day or 21-25 ml hour





Clonidine for Drug Withdrawal

Basic Dosing Scheme

Clonidine 0.1 mg po BID to QID


Rapid PO Detox

Combine with naltrexone




6 mcg/kg/day po divided TID


11 mcg/kg/day po divided TID


0.6 mcg/kg/day po divided TID


Gradual taper or convert to patch


Conversion to Patch




Place patch; give additional 100% po dose


Patch remains; give 50% po dose


Patch remains; give 25% po dose


Patch remains; d/c clonidine po


Alcohol Withdrawal (or chronic BZs)





Medication Conversion


Arterial Blood Gas

Always ask “acute or chronic” and “what is the albumin”

Albumin: For every decrease by one below four, add 7.5 to AG



  1. Internal Consistency


40 ± (| 7.4 – pH |/0.1)  = PCO2/[HCO3]


  1. Acidemia or alkalemia?
  2. What is the primary disorder?



Primary Disorder









Primary Disorder








  1. What is the anion gap


AG = Na – (Cl + HCO3) = 12

Expect 2.5 x albumin


  1. What is the delta gap


Change in AG = Change in HCO3

For every 1 mmol/L rise in AG there should be a 1 mmol/L decrease in HCO3

If not, mixed acid base disorder or lab error


If change in HCO3 > change in AG:

If change in HCO3 < change in AG:

·        Metabolic acidosis

·        Metabolic alkalosis


  1. Is there compensation?





Respiratory Acidosis









Respiratory Alkalosis









Metabolic Acidosis



Metabolic Alkalosis




  1. What is the cause


Metabolic Alkalosis





Starts 24 to 48 hours after ICU admission

TF vs. TPN

What are the residuals?

Before starting TF, add up glucose given in previous day and give half in sauce

COPD: give protein diet (carbs go to CO2 which increase work of breathing


Patients switch to catabolic state on day 3


Morphine, fentanyl, remifentanil

Continuous better than bolus



Thromboembolic prophylaxis

Head of bed

HOB at 45 degrees and move patients up if they have slid down.

Ulcer Prophylaxis


MICU 140’s – 150’s, SICU much tighter

Common Orders

Lab Sets

Hemolysis: Haptoglobin, LDH, Fractional excretion of bilirubin

DIC panel: D-dimer, Fibrin split products




Steroid Use


Tylenol Orders

Medications – IV to PO Conversion


Medications – Steroids

1 mg Dexamethasone equals 5 mg Prednisone which equals 25 mg Hydrocortisone



Ionized Calcium from albumin


Plasma Osmolality =  (2 x Na) + (Glucose/18) + (BUN/2.8)


Osmolal Gap =  Difference between calculated and measured plasma osmolality

(can be used to distinguish acute renal failure (normal) from chronic renal failure (high) or to spot solutes other than sodium, chloride, glucose and urea in the blood (ex. ethanol, methanol, ethylene glycol, other toxins).


For every 100 mg/dL increment in the plasma glucose the plasma sodium should fall by 1.6 to 2 mEq/L.



Tidal volume 6-7 mL/kg (10-15 mL/kg in mechanical ventilation to reduce atelectasis)



SaO2 95%

SvO2 70%

A drop in SvO2 below 70% indicates that systemic O2 delivery is impaired.

A drop in SvO2 below 50% indicates a global state of hypoxia.

SvO2 is measurement requires a pulmonary artery catheter.



Measured via a central venous catheter

When averaged over multiple readings the agreement between ScvO2 and SvO2 is within 5%.



Lactate > 2 mEq/L is abnormal. > 4 mEq/L can be used to predict survival.



1 pound = 0.45359237 kilograms


ICU Radiology

Endotracheal tube:

Thoracostomy tube:

Nasogastric tube

Feeding Tube:

Central Venous Pressure Monitors

Swan-ganz (PCWP)

Intra-aortic Balloon Pump

Electrolyte Replacement

Call HO:


Potassium IV replacement (must have central access)

K level

3.9 – 4.0

3.6 – 3.8

3.3 – 3.5

3.0 – 3.2

Replace with

20 mEq/50 cc each over 1 hour

20 mEq/50 cc x2 each over 1 hour

20 mEq/50 cc x3 each over 1 hour

20 mEq/50 cc x4 each over 1 hour


Potassium PO replacement

K level

3.9 – 4.0

3.6 – 3.8

3.3 – 3.5

3.0 – 3.2

Replace with

20 mEq x 1

40 mEq x 2

20 mEq q2h x 3

40 mEq q2h x 2


Magnesium IV Replacement

Mg Level

1.8 – 2.0

1.5 – 1.7

1.0 – 1.4

Replace with

1 gm

2 gm

3 gm


Magnesium PO Replacement

For Mg level 1.0 – 1.5 give:


Calcium Gluconate IV Replacement

Ionized Ca level

3.5 – 3.9

3.0 – 3.4

2.5 – 2.9


Replace with

9.4 mEq in 100 ml IV over 60 min

14.1 mEq in 100 ml IV over 90 min

18.8 mEq in 100 ml IV over 120 min

23.5 mEq in 100 ml IV over 180 min


Phosphate IV Replacement

For Phosphate level < 2.4:


Answer Calls About Respiratory Status (Katie’s Vent Lecture)


Causes of hypercarbia:


Patients not on a ventilator





Patients on a ventilator

Peak Inspiratory Pressure (PIP) = Central + Parenchymal Pressure


Parenchymal pressure is compliance and can be measured as the pressure at a pause at the end of respiration, called Plateau Pressure.


If the Peak Inspiratory Pressure is elevated but the Plateau Pressure is not then this is a central problem.

If both the Peak Inspiratory Pressure and the Plateau Pressure are elevated then this is a parenchymal problem.


Central problem


Parenchymal problem (compliance)



Causes of hypoxia:


Factors we can change to affect hypoxia



FiO2 is toxic at high levels, but in the acute situation don’t worry about that. Raise it as much as you need to oxygenate the patient.



PEEP can cause parenchymal damage at high levels. We can be more liberal with PEEP when there is diffuse lung injury. When there is a localized problem (ex. lobar PNA) the PEEP will preferentially be shunted to the normal (low pressure) lung.



Auto-PEEP occurs in patients with obstructive disease such as COPD or asthma. You add their auto-PEEP to ventilatory PEEP to obtain the total PEEP. Watch for breath stacking. When breath stacking occurs peak pressures begin to climb in a step-wise fashion. This occurs because the obstructive patient is not being given enough time to exhale. Change the I:E ratio (ex. 1:2) to allow for complete exhalation.


Respiratory Distress Checklist



Tube moved


Biting on tube

Check tube

Vent tubing/O2 connected

Check vent and O2 setup


CXR/Clinical suspicion

Flash pulmonary edema

High prior BP

Heart failure/MI

I/Os, Hypotension




RR low, brainstem reflexes

Metabolic acid-base compensation

RR increasing

Muscle fatigue

Accessory muscles, tripoding


Auscultation, suctioning

Vocal Cord Dysfunction


Alveolar Hemorrhage

CXR? Bronch





On Call Responsibility


Call-outs (Transfers)




Admission Note




  1. Pulmonary: Respiratory Failure, intubated for airway protect, ARDS
    1. Intubation

                                                               i.      Sedation

                                                             ii.      Weaning

                                                            iii.      CXR for ET tube placement

    1. ARDS

                                                               i.      Low TV and limitation of inspiratory plateau pressure strategy for ALI/ARDS

                                                             ii.      Conservative fluid use if not in septic shock

    1. Albuterol/Nebs as needed
  1. Septic shock with MOD, 4/4 SIRS criteria now awaiting cultures
    1. HD stable on pressors
    2. Wean fluid as pressure stablizes
    3. Follow-up cultures
    4. Consider stress dose steroids if pressure becomes unresponsive to fluid and pressors
  2. Metabolic Acidosis 2/2 sepsis with elevated lactate
    1. Adjust vent settings so patient is breathing above vent
    2. Follow-up lactate
  3. ID
    1. Follow up on cultures
    2. Continue ABX (Vanco, zosyn, flagyl)
    3. Identify infectious source

                                                               i.      CXR

                                                             ii.      CT ab/pelvis

                                                            iii.      US ab/renal

  1. CV
    1. Holding home CV meds for shock
  2. AMS
    1. Likely due to septic shock
    2. CT head for possible hemorrhage
  3. Renal:
    1. Acute Renal Failure

                                                               i.      Fluid resuscitation with goal UOP of 0.5 ml/hr

    1. Foley Catheter
    2. ICU electrolyte protocol
  1. Heme
    1. Target hemoglobin 7-9 g/dL (no history of CAD)
    2. Type and screen q72h
  2. Endocrine
    1. Regular Insulin gtt to maintain blood glucose at 150
    2. No steroids (unless patient has history of steroid use or is known adrenally insufficient)
  3. PPX
    1. Protonix (intubated)
    2. HOB at 30 degrees while ventilated
    3. IPC stockings (Heparin SQ once cleared for hemorrhage? CT head?)
  4. Nutrition
    1. NPO until further notice


Common Orders

GI Prophylaxis

Taking PO: Protonix 40mg po qday

Unable to take any PO and no NG: Protonix 40mg IV Qday

NG Tube in place: Omeprazole/Na Barb 20mg PT qday











Vasopressin 0.01 U/min

No titration order










Free Text Respiratory Order