Bugando Medical Center

Adult Intensive Care Unit

Resident and Student Manual

2011
Part I: AICU Expectations

Introduction:
The Adult Intensive Care Unit (AICU) provides intensive medical management of
critically ill patients at Bugando Medical Center. Patients admitted to the medical,
surgical and obstetrics/gynecology services can be cared for in the AICU. The Medical
ICU team is the only service based in the AICU and will assist with medical management
of all AICU patients including surgical, pediatric and OG patients as necessary.

AICU expectations for residents and students:
The care team in the ICU is composed of a specialist, senior resident, junior resident,
registrar, medical students and nurses specializing in critical care.
All residents and students should arrive in the AICU before 7 am Monday thru
Friday to pre-round on their patients.
Residents and students should arrive before 9am on Saturdays for pre-rounds.
Sunday only residents are in the AICU.
Each patient in the AICU must have a student or resident who is primarily
responsible for their care. New patients should be picked up by a member of the
team. If a patient does not have a primary care giver, the senior resident will
assign one.
Pre-rounds consists of reviewing overnight events with the nursing staff,
reviewing vital signs from overnight, reviewing new test results, interviewing,
examining the patient and writing your complete note including the plan for the
day described by problem.
If any patient care interventions must be done urgently for critically ill patients,
they should be done at this time in consultation with the AICU resident.
Residents and students are expected to attend conference at 8am.
Rounds with the AICU specialist begin at 9:30am and all of the team should be
available in the AICU at this time.
All patient notes, including impression and plan, should be written before AICU
rounds with the specialist.
All notes written by students must be reviewed and countersigned by the
responsible resident in the AICU.
Residents and students are responsible for the completion of all components of the
plan on patients in the AICU including; lab tests, imaging tests, procedures,
ordering and ensuring administration of medications and consults.
Residents and students should review each patient throughout the day to check on
the patients condition after any intervention and follow-up the results of any
tests. Any adjustments can be made to the plan based on these assessments.
Formal afternoon rounds will occur at 4PM every afternoon with the AICU
residents and students together with the on-call medicine resident to review all
patients and make any necessary changes in plan.
For every patient that dies in the AICU, the family should be immediately
contacted to request an autopsy.
Part II: Daily Presentation on Attending Rounds

Presentations in the AICU follow a different format than on the wards. They must be both thorough and
succinct. You must present a lot of information and it helps to present it in a standardized format to ensure
nothing is missed. Please use the following format when presenting patients on AICU rounds and when
writing your daily progress notes. We hope that this system will help you to develop a systematic way for
presenting ALL inpatients, whether in the AICU or on the wards, so that you can you will not forget
important details of the patients progress or management.

Subjective
1) Provide a one line summary of the patients medical problem that brought them to the ICU. (ie. This is a
55 year old man who presented two days ago with variceal bleeding and hypovolemic shock.)

2) Review events of previous 24 hours (e.g. procedures, intubation, extubation, spontaneous breathing
trials, hypotension, fever, recommendations of consult services)

3) Patients subjective complaints/report

Objective
4) Vital Signs
Maximum temperature in the last 24 hrs and the current temperature
Current BP, the BP range/trend over last 24 hours. Current pulse
Respiratory rate, oxygen saturation and amount of supplemental oxygen

5) For patients on a ventilator: Current vent settings: Mode of ventilator, Tidal Volume, RR set on machine,
PEEP, pressure support, FiO2, peak airway pressure

6) Total amount in and out past 24 hours. Urine output last 24 hours. Type and amount of nutrition.

7) Last 4 Finger sticks (if applicable)

8) Physical examination. Pay particular attention to changes in the patients physical exam. All affected
systems should be presented completely. Other systems can be presented as normal of they are normal or,
if abnormal, should be presented completely.

9) Laboratory investigations and results. If tests were sent and are pending, report the day the test was sent
and if it the lab confirmed that the sample was received. Include bedside test results (urine, rapid test etc.)
which should be done during pre-rounds if important.

10) Imaging results (x-ray, ultrasound; report any pending tests that have been ordered and not performed).
Any bedside ultrasound reports should also be reported in this section. Bedside ultrasound should be done
as part of pre-rounding if indicated.

11) List each current medication including the dosage, schedule, duration and the reason you are
prescribing it. Include current medication infusions and their rates. All ionotrope/vasopressor drips (like
epinephrine, dopamine and dobutamine) should be reported as micrograms/min and not just mL/min. Also
report type, amount and rate of IV fluid given in the last 24 hours remembering that IV fluids are
medications.

Assessment:
12) Impression: list the patients current problems in order of importance (the problem that is life
threatening or the reason they are in the ICU should come first). Most patients in the ICU have multiple
problems. After listing all of your impressions/problems you should also list any important differential
diagnoses. Be ready to discuss each impression/differential briefly including the reasons for each
impression and differential.

Plan:
13) Plans must be organized by impressions/problems. Give the details of your plan for each problem
listed in your impressions. This is extremely important as it will teach you how to manage each individual
problem in complex patients, a learning point that will also be applicable to ward patients with similar
problems.
Example: Impression - Hypovolemic shock 2/2 variceal bleeding
- Urgent control Hb
- Blood Transfusion 2 units STAT
- Full Blood Picture
- Hepatitis B and C serologies
- Continue Octreotide drip at 25 micrograms/hr
- Continue epinephrine infusion at 1mcg/min to maintain MAP>65, wean as
tolerated
- Monitor Urine Output
- Continue Ranitidine IV 50mg BD
- NPO
- Hold patients home antihypertensive medications
- Schedule endoscopy when patient is hemodynamically stable.
- Give praziquantel 20mg/kg 6hrly X4 when taking PO

14) In addition the problems listed in your impression, a plan for the following categories MUST be
addressed on ALL ICU patients daily.
Fluids, electrolytes and nutrition (FEN)
Prophylaxis
- DVT prophylaxis (heparin 5000 units subQ BD or contra-indication)
- GI prophylaxis (for intubated patients, severe neurologic injury, high dose steroids, GI bleed)
- Head of bed elevated/not elevated at 45 degrees
Disposition (stay in ICU, stable for transfer to the ward)

Part III: Critical Care Curriculum

Bedside Ultrasound

The AICU has its own portable ultrasound machine that is available for use by residents in the AICU.
Bedside ultrasound is a powerful tool for real-time assessment of critically ill patients, and can help you
make informed decisions for the appropriate treatment of patients with complex medical problems. It can
supplement your history and physical exam skills when differentiating between many clinical conditions
such as types of shock or periportal fibrosis vs cirrhosis. Bedside ultrasound is only as good as the person
operating the machine and interpreting the images. Take advantage of your rotation in the ICU to build
your skills performing and interpreting bedside ultrasound.

Please ensure that the ultrasound machine is plugged-in and stored in the Doctors Room of the AICU
when it is not in use, and that the ultrasound probe is cleaned thoroughly after use and between patients.

Important indications for use of bedside ultrasound in critically ill patients:
Evaluation of volume status in septic patients by assessment of IVC variability
Assessment of liver parenchyma, congestion, and portal vein
Assessment of gall bladder
Evaluation and localization of pericardial effusion and tamponade
Rough assessment of cardiac function
Evaluation of pleural effusion and marking for thoracentesis
Assessment of ascites and marking for paracentesis
Measurement of splenomegally
Assessment of kidneys, ureters and bladder in patients with renal failure
Evaluation for free fluid/blood in abdomen in trauma patients (ie FAST scan)
Placement of IV catheters in patients with difficult IV access

In patients with one of these indications for bedside ultrasound at the time of pre-rounding, ultrasound
should be performed before rounds so that the findings can be reported to the Specialist Physician at the
time of rounds. It is important that it is done before rounds to maximize both patient care and learning.
Based on your experience and confidence, the Specialist may chose to confirm your findings. Bedside
ultrasound, of course, may also be performed at any other time of the day and night and will be expected as
part of morning report presentations for patients with the above indications.

Basic ultrasound skills all residents should be competent in performing and interpreting by the end
of their ICU rotation:
Localization of IVC and assessment of the respiratory variability of the IVC as a marker of
volume status.
Localization of the heart, and assessment of pericardial effusion. Measurement of pericardial
effusion.
Localization of the kidneys and bladder. Assessment for hydronephrosis.
Assessment of pleural effusion.
Assessment of ascites.
Assessment of liver parenchyma.

Airway Management

The first priority in managing any critically ill patient is to secure the airway. Foreign bodies can obstruct
the airway as occurs during choking on food (treated with the Heimlich maneuver or extraction with
forceps). The most common cause of airway obstruction in an unconscious patient, however, is occlusion
by the tongue and soft tissues of the pharynx. The following protocol enumerates steps to maintain a patent
airway in an unconscious patient. This protocol emphasizes manual ventilation and delays endotracheal
intubation until adequate pre-oxygenation and ventilation have been performed. One of the most common
errors made by physicians in emergency situations is proceeding directly to endotracheal intubation without
first establishing a temporarily secure airway and manual ventilation.

Unconscious Patient with Stable Cervical Spine

I) Determine if airway is patent by physical examination
- Assess for stridor
- Assess if chest wall rises and falls with each breath
- Assess breath sounds

II) If airway is patent
- Provide supplemental oxygen if indicated
- Continue with general assessment of patient

III) If airway is not patent or inadequate spontaneous breathing
- Head tilt and chin lift to open airway
- Set up suction apparatus and suction catheter
- Attach bag-valve mask (BVM) to high flow (10L/min) oxygen
- Place BVM over patients face
- Press down with your thumbs on cephalad portion of mask against the bridge of the nose
- Press down with your index fingers on the portion of the mask covering the chin
- Gently lift the mandible anteriorly with your remaining three fingers on each hand
- A second operator compresses the bag to deliver tidal volume
- Adequate ventilation occurs when the chest wall rises with each breath delivered and condensation forms
in the mask upon exhalation. Excessive amounts of air should not leak out from the sides of the mask.
- Ventilate at appropriate rate: e.g. 20/min if patient has severe metabolic acidosis or at slower rate (e.g.
12/min) if patient has chronic CO2 retention. Prevent auto-PEEP by allowing complete exhalation prior to
delivery of next breath
- Coordinate manual ventilation with patient effort if s/he is breathing spontaneously

IV) If chest wall does not rise with manual ventilation
- Repeat head tilt and chin lift
- Reposition seal with mask and re-attempt manual ventilation

IV) If chest wall still does not rise with manual ventilation
- Temporarily remove BVM and inspect airway for secretions or foreign bodies
- If no foreign bodies found, place an appropriate sized oral pharyngeal airway (should reach from tragus to
ipsilateral angle of the mouth when held against the side of the face). The oral airways curved tip should
face the palate during insertion. Advance the oral airway between the palate and tongue until approximately
2/3 of it lies within the mouth. Next, rotate the oral airway 1800 around its long axis so that the curved tip
points caudad. Advance the oral airway until the proximal end lies anterior to the teeth and the distal end
lies posterior to the tongue. A properly placed oral airway prevents the tongue from occluding the airway.
- Repeat head tilt/jaw lift and replace BVM with a good seal


II) The above steps should secure the airway and provide adequate ventilation in the overwhelming
majority of patients
- Manually ventilate the patient until he/she is adequately pre-oxygenated and someone skilled in intubation
is present and has equipment properly assembled
- If you cannot manually ventilate a patient with a BVM, a true airway emergency exists. Get as much help
as possible and proceed to endotracheal intubation

Shock
Shock is a syndrome of acute circulatory failure associated with ineffective tissue perfusion and
cellular injury.

Cellular injury manifests as multi-system organ dysfunction which is initially reversible. Persistent shock
leads to irreversible organ failure and death. The physiological derangements of shock include circulatory
failure, microvascular and endothelial dysfunction, and dysregulation of the clotting and inflammatory
cascades. Cellular homeostasis fails and cells lose their ability to perform work and ultimately die.

Understanding shock requires an understanding of the normal circulation.

Cellular homeostasis requires constant perfusion.
The circulation provides oxygen, nutrients, immunoglobulins and the chemical mediators of cellular
function and carries away CO2, products of metabolism and mediators of cellular interactions. Cells require
large amounts of energy to perform work and create organization. Cells, for example, consume one third of
their ATP by pumping sodium against its concentration gradient to maintain tonicity, size and membrane
potential.

Adequate perfusion requires sufficient quantities of blood constituents. Consider oxygen delivery.
Every gram of fully saturated hemoglobin carries 1.34 ml of oxygen. The content of oxygen in arterial
blood (CaO2) is determined by:
CaO2= 1.34 x Hgb x SaO2
If the hgb is 15gm/dl and SaO2 is 100% then the CaO2 is 20mlO2/dl blood. Using this equation you can
calculate the effect of anemia or hypoxemia on oxygen carrying capacity.

Adequate perfusion requires sufficient cardiac output (CO). The determinants of cardiac output are
CO = Pulse x Stroke Volume

The normal CO is 5 L/min

Cardiac index (CI) is CO indexed to body surface area (BSA)
CI = CO/BSA (normal CI > 2.5 L/min/m2)

Catecholamines and the autonomic nervous system regulate heart rate.

The Frank-Starling law describes the determinants of stroke volume: intrinsic myocardial
contractility and the ventricular loading conditions.

Stroke volume varies with changes in preload at lower filling volumes. Preload is the ventricular end-
diastolic volume (LVEDV & RVEDV) which helps determine the myocyte stretch preceding contraction.
Volume depletion tends to decrease stroke volume. Increased intrinsic contractility shifts the curve upward
(as occurs with endogenous or pharmacological inotropes). A decrease in after-load also shifts the curve
upward. The curve is shifted downward by increased after-load or decreased intrinsic contractility (systolic
dysfunction). If left ventricular end diastolic pressure is plotted on the x-axis (LVEDP) than the curve is
also shifted downward by decreased myocardial compliance diastolic dysfunction.






The above graph is an idealized representation. Many doubt the presence of a decrease in SV from
ventricular over-distention at high LVEDV.

Clinicians are unable to measure LVEDV directly. Ventricular filling pressures are common clinical
correlates of preload. They are:

a) Central Venous Pressure (CVP): this is the pressure in the right atrium and is obtained by transducing
any neck vein catheter or measuring the jugular venous pressure

b) Pulmonary Capillary Wedge Pressure (PCWP): This value is obtained by pulmonary artery
catheterization estimates the left atrial pressure which approximates left ventricular end diastolic pressure
which estimates left ventricular end diastolic volume (LV preload) .

Low filling pressures suggest that a low cardiac output is due to intravascular volume depletion. However
filling pressures do not often approximate LVEDV due to many factors (abnormal ventricular compliance,
valvular heart disease, positive pressure ventilation and technical difficulties with the measurements.)

A pulmonary artery catheter can measure cardiac output by thermodilution. Room air saline is
injected into the right atrium via a side port in a pulmonary artery catheter. A thermistor at the distal tip of
the catheter measures the fall and recovery of the temperature of blood in the pulmonary artery. The area
under the idealized thermodilution curve is proportional to the cardiac output. Tricuspid regurgitation adds
error to this calculation because cooled blood flows back up into RA with RV systole


The Fick method can also measure cardiac output.
The Fick method states that the rate of oxygenated blood flow away from the lungs is equation to the rate
of oxygenated blood flow to the lungs plus the rate of oxygen added to blood from inspired air by the lungs.
The rate of oxygen flow away from the lungs is equal to the cardiac output (Q) times the content of oxygen
in arterial blood (CaO2). The rate of oxygen flowing to the lungs is equal to the cardiac output (Q) times
the content of oxygen in mixed venous blood in the pulmonary artery (CvO2). The figure below is a
schematic representation of the flow of oxygen through the system.

Using mass spectrophotometry, a metabolic cart can analyze inhaled gas to determine the rate of oxygen
removed from inspired air by the lungs (called oxygen uptake VO2). Clinicians calculate CvO2 and CaO2
from samples taken from the pulmonary and systemic arteries.
CaO2 x Q = CvO2 x Q + VO2
Therefore:
Q = VO2/CaO2 CvO2

Stated another way: Cardiac output equals the rate of oxygen uptake by the lungs divided by the arterial-
mixed venous oxygen difference.

Adequate perfusion requires an appropriate distribution of blood flow. Mediators such as
catecholamines, NO and ADP influence the relative perfusion of capillary beds. Normally 20% of the
cardiac output is directed to the kidneys. A normal cardiac output can be insufficient to sustain normal
renal function if flow is diverted away from the glomerular capillary beds. This situation happens in
hepato-renal syndrome in which an increased cardiac output is shunted away from the kidneys. In shock,
endothelial dysfunction, and sludging of the microcirculation with neutrophils, sloughed endothelial cells
and fibrin impair perfusion.

Adequate perfusion requires efficient transfer and utilization of oxygen.
In sepsis, cells may be unable to utilize the delivered oxygen. This process, called cytopathic hypoxia, may
be due to inflammatory up-regulation of P(ARP)-1 polymerase which depletes cytoplasmic NAD, a
limiting reagent of oxidative phosphorylation. Cells therefore, may be unable to synthesize sufficient ATP
despite adequate cellular oxygen.

Clinical Assessment of Perfusion


Surrogate Markers of Perfusion
Clinical Indices of Oxygen Delivery
Blood Pressure DO
2

Urine Output SvO
2

Pulse Lactate Concentration
Capillary Refill
Absence of Encephalopathy
Acidosis/Base excess/ Anion Gap

Blood pressure is the most commonly used marker of perfusion. It is governed by

BP = CO X Systemic vascular resistance

BP, therefore, is also proportionate to stroke volume and pulse. BP reflects the perfusing force of blood in
the large arteries. However blood pressure is an unreliable indicator of perfusion in the microvasculature.
Healthy young people with severe hypovolemia can have significant hypoperfusion even though their BP is
maintained by catecholamine induced compensation (raising pulse and SVR). Similarly patients with shock
whose blood pressure is normalized with vasoconstrictors can suffer from severe hypoperfusion of the
microcirculation. Catecholamines constrict arterioles which are upstream from the capillaries which can
remain under-filled. However, a mean arterial pressure of 60mmhg or a drop in systolic BP of 30mmhg
from baseline is generally suggestive of hypoperfusion.

Indices of oxygen delivery as surrogate markers of perfusion
Oxygen delivery (DO2) is governed by:

DO2 =CO x CaO2

CO is cardiac output and CaO2 is the content of oxygen in arterial blood and is determined by: 1.34 ml O2
x Hgb x SaO2

Therefore: DO2 = CO x 1.34 ml O2 x Hgb x SaO2

Substituting in the normal values (CO=5L/min at rest, Hgb 15gm/dl, 100% saturation) we find that the
normal resting oxygen delivery approximates 1000 ml/min. The normal total oxygen consumption (QO2) is
250 ml/min. The cells are totally dependent on the circulation to provide oxygen for consumption in
metabolism. Therefore if the DO2 drops below a critically low value there will be insufficient oxygen
available to generate energy. In healthy anesthetized individuals the critical value is around 300ml/min of
DO2.
Above this critical threshold DO2 can drop extensively and a compensatory increase in the relative
extraction of delivered oxygen will maintain QO2. The mechanism of the increased extraction is likely
related to local tissue effects such as a decrease in pH causing oxygen to offload from hemoglobin.
Obviously shock occurs if DO2 falls below the critically low value. The stressors of critical illness such as
fever and high work of breathing raise VO2 requirement. One model of shock suggests that patients may
not be able to efficiently increase oxygen extraction to meet the demand of increased QO2 and therefore
patients in shock require high levels of DO2. Indeed, survivors of critical illness have higher DO2 values.
Clinicians therefore often attempt to augment DO2 by increasing its constituents (CO, Hgb, and SaO2) to
keep it above its critical value. There is no way to determine critical DO2 and therefore clinicians often use
the oxygen saturation of mixed venous blood (SvO2) to determine if DO2 is adequate.

SvO2 is an indirect marker of oxygen delivery and perfusion
SvO2 or mixed venous oxygen saturation refers to the oxygen saturation of pulmonary arterial blood.
SvO2 reflects the oxygen left over in venous blood after the tissues extract the oxygen they need from
blood in the capillaries. This saturation of venous blood varies depending on the capillary bed of origin. For
example venous blood returning from the glomerular capillary beds of the kidney have a much higher
oxygen saturation then blood returning from the brain. When venous blood reaches the pulmonary artery it
is fully mixed and therefore the SvO2 represents the average oxygen saturation of all the venous blood.
SvO2 reflects the balance between the amount of oxygen delivered and what is consumed. At rest and a
normal DO2 the SvO2 is around 70%. If the DO2 is relatively low compared to QO2 then the extraction
ratio will be high and SvO2 will be low. Therefore a low SvO2 is often used to determine if DO2 is low in
shock states (as occurs in cardiogenic shock or severe hemorrhage). There are multiple problems with using
SvO2 to assess adequacy of perfusion. One is that is that SvO2 is very low in normal healthy exercise.
Another is that its measurement requires a pulmonary catheter. Moreover SvO2 can be normal in
vasodilatory shock. Therefore many clinicians use other markers to assess the adequacy of perfusion

End-organ function as surrogate markers of perfusion. In the presence of hypotension or a clinical
scenario that may cause shock (e.g. major hemorrhage or infection) clinicians look for shock induced organ
dysfunction.

Important abnormalities include:
Respiratory system: Patients in shock will be tachypneic or in respiratory distress even if oxygenation is
normal. Minute ventilation increases in response to the metabolic acidosis of shock, but a respiratory
alkalosis will also occur due to cytokines and hypoperfusion of medullary receptors. Hypoperfusion of
respiratory muscles at a time of increased demand can lead to respiratory failure requiring intubation to
prevent sudden death. As shock progresses, ventilation/perfusion mismatches and non-cardiogenic
pulmonary edema from endothelial dysfunction commonly cause severe hypoxia (ARDS).
Renal: oliguria (<1/2 ml/kg/hr) is an important early sign of hypoperfusion (except for patients who have
oliguric renal failure prior to the onset of critical illness). As shock progresses acute tubular necrosis and
acute renal failure may develop.
Metabolic acidosis: due to accumulation of lactate and/or other unmeasured anions.
CNS: encephalopathy manifested as agitation or obtundation
Other abnormalities are common but are less useful for immediate assessment. They include:
ischemic hepatopathy (shock liver), ileus, erosive gastritis, pancreatitis, myocardial depression,
coagulopathy, thrombocytopenia, hyperglycemia, immune dysfunction

Classification of Shock
Four categories

I) Hypovolemic shock: The hallmark of hypovolemia is the loss of intravascular volume leading to
decreased ventricular preload. Decreased preload reduces stroke volume which reduces cardiac output. The
BP equation predicts that the compensatory mechanisms to maintain perfusion are tachycardia and elevated
SVR. Therefore, the patient in hypovolemic shock will be cool and clammy due to peripheral
vasoconstriction.

The classic hemodynamic profile of hypovolemic shock is decreased CVP, PCWP, CO, SvO2 and
increased SVR.

Hypovolemic shock is caused by hemorrhage or fluid loss (GI losses, or loss of fluid into the interstitial
space such as occurs in pancreatitis, traumatic tissue injury and sepsis).
In hemorrhagic shock the fluid deficit exceeds the amount of shed blood. This is because the
hypoperfused cells are unable to maintain their resting membrane potential. Sodium flows into the cells as
the ion pumps fail causing intracellular fluid sequestration. This causes severe interstitial fluid deficit which
tends to pull more fluid out of the intravascular space. Survival depends on administration of large volumes
of crystalloid in addition to blood.
If prompt fluid resuscitation is not administered the patient can develop an irreversible shock state.
At that point no amount of fluid or blood resuscitation will correct the hemodynamic collapse. Irreversible
shock is characterized by severe and persistent vasodilatation and reduced cardiac output

II) Cardiogenic Shock .The primary disturbance is an inadequate cardiac output despite adequate preload.
In fact, the filling pressures are usually pathologically elevated resulting in JVD and pulmonary edema
(typically occurring when PCWP is > 19 mmHg). The BP equation predicts an elevated SVR as the
compensation for decreased CO; therefore, the skin will be cold and clammy. The typical hemodynamic
profile is elevated CVP, PCWP, SVR and decreased CO and SvO2.
Etiologies include massive MI, cardiomyopathy, acute valvular disease, tachycardia and
bradycardia.

III) Obstructive shock Many consider this a variant of cardiogenic shock. The primary disturbance is a
low cardiac output due to an obstruction of diastolic filling (e.g. tension pneumothorax, pericardial
tamponade, high intrathoracic pressures from positive pressure ventilation or an outflow tract obstruction
(massive pulmonary embolism).
The typical profile is decreased CO and SvO2 and elevated SVR and CVP. PCWP may be
elevated but may be normal with pulmonary emboli.

IV) Vasodilatory shock also called distributive shock. The primary circulatory disturbance is decreased
SVR. This failure of vascular smooth muscle contraction occurs despite extremely elevated levels of
endogenous catecholamines and can persist despite infusions of massive doses of exogenous
catecholamines (i.e. vasopressors). The pathogenesis of this phenomenon includes activation of ATP
sensitive potassium channels in vascular smooth muscle as well as vasopressin deficiency and elevated NO
activity (see Landry and Oliver N Engl J Med 2001; 345:588-595, 2001).
The causes of vasodilatory shock include sepsis, pancreatitis and anaphylaxis. Importantly,
vasodilatory shock is a common endpoint of prolonged shock of any etiology such as massive hemorrhage
or after prolonged cardiopulmonary bypass or cardiac arrest.
Because of vasodilatation and loss of intravascular fluid to the interstitium (capillary leak), most
cases are initially complicated by hypovolemia which can diminish CO. Volume resuscitation can restore
preload and allow the typical compensation for vasodilatation: increased CO. The patient in vasodilatory
shock will be warm and flushed (due to peripheral vasodilatation) and have a hyperdynamic precordium.
Prolonged vasodilatory shock results in progressively diminished cardiac function in part due to
myocardial under perfusion and circulating myocardial depressant factors (including TNF).
The typical profile of vasodilatory shock is decreased SVR, and elevated CO (if volume resuscitated). CVP
and PCWP vary depending on volume status. SvO2 may be normal in vasodilatory shock as DO2 is often
elevated and the tissues are unable to utilize the delivered substrate.

Management Of Shock

1) Secure airway
2) Guarantee adequate oxygenation and ventilation
3) Resuscitate circulation
Large bore IV access
Crystalloid
Monitor adequacy of resuscitation
4) Continuous presence of trained clinician at bedside
5) Vasopressors if shock is refractory to fluids
6) Treat underlying cause

Prompt recognition of shock and diagnosis of its etiology are essential if the patient is to survive.
The airway must be secured. Supplemental oxygen is given for hypoxemia. If respiratory distress or severe
acidemia is present the patient will require mechanical ventilation to assume the work of breathing. Nearly
all patients require a Foley catheter to follow hourly urine output, continuous cardiac and oxygen saturation
monitoring, and most will require an arterial line. CVP monitoring is a flawed measure of fluid
responsiveness but indicated if patient is hemodynamically unstable.
Survival requires prompt and adequate fluid resuscitation. In general administer isotonic
crystalloid (LR or NS) in 500ml-1L boluses and re-evaluate the patient after each fluid bolus to determine
response. Most patients with vasodilatory shock will require 4-5 L of volume in the first few hours (and
may ultimately require three times this amount). For severe hemorrhage a general guide is 3ml of
crystalloid for every 1ml of shed blood. Warm the fluid prior to transfusion of crystalloid and blood
products to prevent hypothermia.
Typical end points of volume resuscitation include restoration of blood pressure without the need
for vasoconstrictors and restoration of normal urine output (although urine output may not correct if patient
is in oliguric ATN). For hemorrhagic shock many ICU doctors continue volume resuscitation until the
acidosis is corrected. For sepsis consider normalization of SvO2 or oxygen saturation of central venous
blood (ScvO2) during first 6 hours of resuscitation. Variation of the inferior vena cava diameter or systolic
pulse pressure with the respiratory cycle may predict responsiveness to fluid resuscitation. These measures
are more reliable then the traditional filling pressures of CVP <12mmhg and PCWP <19.
Other end points include evidence of pulmonary edema or markedly elevated filling pressures.
Patients in cardiogenic shock should receive much more cautious fluid boluses (100-200cc) or none at all if
there is evidence of pulmonary edema.
Although it remains controversial we do not routinely resuscitate patients with colloid. An
exception is blood transfusion.
Correct choice of intravascular catheters is essential. Flow through the catheter is independent of
the size of the vein but inversely proportional to the length of the catheter. Flow is proportional to the
fourth power of the radius of the catheter. Therefore short, large bore catheters are essential for rapid fluid
administration. For example:
22 gauge angiocath: maximum infusion rate: 35 ml/minute
20 gauge angiocath: maximum infusion rate: 60 ml/min
18 gauge angiocath: maximum infusion rate: 105 ml/min
16 gauge angiocath: maximum infusion rate: 205 ml/min
14 gauge angiocath: maximum infusion rate: 333 ml/min
Therefore, small IV's are inadequate for rapid volume resuscitation. Long triple lumen central lines may
also be inadequate (large lumen allows 34 ml/min, other two lumens each allow 17 ml/min). Large bore are
ideal. Electric pumps will slow infusion rates through large bore catheters (maximum rate 1L/hr). Rapid
infusions require only gravity and plain IV tubing.

Monitor and treat complications of massive fluid resuscitation; this is especially important in bleeding
because massive resuscitation causes hypothermia, hypocalcaemia, and dilution of clotting factors all of
which worsen coagulopathy. Treatment of hemorrhagic shock can lead to a vicious cycle of massive
transfusion leading to worsening coagulopathy and therefore more bleeding. Infuse thawed plasma (FFP)
when bleeding is severe enough to require massive transfusion (>4units PRBC).

Complications of Massive Resuscitation

Fluid Overload Causes of Coagulopathy
Decreased respiratory compliance Hypothermia
Pulmonary Edema Dilution of clotting factors
Abdominal compartment syndrome Hypocalcemia

Complications of Normal Saline Complications of PRBC
Metabolic acidosis Viral infection (very rare)
Hypernatremia Nosocomial Pneumonia
Hypokalemia



Prompt treatment of the underlying cause of the shock is essential: antibiotics and drainage of infected
foci for sepsis, thrombolysis for PE, pericardiocentesis for tamponade, control of bleeding, re-perfusion
therapy in acute MI, tube thoracostomy for tension pneumothorax, cardioversion of arrhythmias. Other
therapies in the literature that are not currently available at BMC include placement of intra-aortic balloon
pump or left ventricular assist device for refractory cardiogenic shock, and using activated protein C for
patients in septic shock (Bernard, NEJM 344; 20001: 699-709). Consider low dose steroid replacement
(JAMA 288; 2001:862-871) and early normalization of hemodynamic variables (i.e. ScvO2, CVP, UO, and
BP as in NEJM 345; 2001: 1368-1377) for septic shock. Consider low tidal volume ventilation if the
patient develops ARDS (NEJM 2000; 342: 1301-1306).

Vasoactive drips: There is little evidence from clinical trials to guide the use of vasoactive drips.
Vasoconstrictors can restore the blood pressure to a normal value without normalizing perfusion and they
do not correct the misdistribution of blood flow that characterizes shock. Vasoactive drips should never be
used in place of adequate volume resuscitation or treatment of the underlying etiology of the shock. The
patient who is on these vasoactive drips is unstable and the clinician should constantly attempt to liberate
the patient from the drips. Nonetheless experience suggests these medications can be life-sustaining in
patients in shock.
Vasoactive drips target various receptors:
Alpha
Beta Predominantly found in heart; activation causes increased inotropy and chronotropy
Beta2
Dopaminergic: One subtype causes vasodilatation of splanchnic, cerebral and coronary vasculature; another
subtype causes vasoconstriction

Drips currently available in the BMC AICU:
Dopamine dose responses for various receptors vary;
1-3 mcg/kg/min dopaminergic receptors predominate with dilation of renal and splanchnic vessels. Some
vasodilatation and tachycardia
5-
>10 mcg/kg/min: alpha predominates with some Beta activity
In summary, at mid doses dopamine causes tachycardia and modest increase in CO.
Vasoconstriction increases with increased dose. Controversy exists over the use of renal dose dopamine (1-
3 mcg/kg/min) to preserve renal perfusion. Dopamine does increase urine output at low doses that is likely
transient and due to naturesis. However, it is relatively certain that it does not improve renal function
(GFR) or mortality [Lancet 356; 2000]

Epinephrine At low doses epinephrine activates receptors and alpha. The net result is increased CO with
variable vasoconstriction and effect on BP. At higher doses alpha effects predominate increasing
vasoconstriction and BP. Epinephrine is the drug of choice for anaphylaxis.

Dobutamine Potent stimulator of receptors increases cardiac output and vasodilatation. Commonly used
in cardiogenic shock (characterized by decreased CO and high SVR) its effects include vasodilatation and
hypotension as well as tachyarrhythmias. Long-term inotropic support increases mortality; it is presumed
that short-term isotropic support does not increase mortality although there is no clinical trial data to
support this. You can add dobutamine to other vasoconstrictors if additional cardiac output needed to
augment perfusion. Start at 2.5mcg/kg/min if no adverse effects increase to 5mcg/kg/min, if the patient
tolerates this dose but inadequate response increase to 7.5mcg/kg/min. Dobutamine can lower blood
pressure because of its vasodilatory properties and must be used in concert with another vasopressor in
hypotensive patients.

Other Important Vasopressors not currently available at BMC
Norepinephrine (Levophed) potent alpha agonist (vasoconstrictor) also some B activity which may
increase CO. Used in vasodilatory shock, it is a commonly used vasopressor in septic shock.

Phenylephrine (Neosynephrine): Pure alpha agonist causes vasoconstriction (increases SVR). May cause
reflex bradycardia. Useful in vasodilatory shock especially in setting of tachyarrhythmia.

Vasopressin Used in vasodilatory shock to replace vasopressin deficiency and cause vasoconstriction. May
preserve renal perfusion. Can decrease CO as well as cause hyponatremia.
Mix 25 units/250cc D5W infuse at 0.04 units/minute (24ml/hour), do not titrate to higher dose; must taper
off slowly.

Introduction to Mechanical Ventilation

I) Normal Negative Pressure Ventilation
During inhalation diaphragmatic contraction increases intra-thoracic volume which reduces intrathoracic
pressure (also called pleural pressure). Air flows down its pressure gradient and fills alveoli. Greater effort
reduces pleural pressure further and increases airflow. During exhalation pleural pressure rises which
drives air out of the thorax.

II) Positive Pressure Ventilation: The ventilator interfaces with the patient via a facemask, endotracheal
tube or tracheostomy tube. These create a nearly closed circuit between the ventilator and the patients
airways. The ventilator blows air in through the inspiration limb; during exhalation the inspiration port
closes and the exhalation limb opens.
Effects of positive pressure ventilation (regardless of mode)
Recruit atelectatic alveoli which can decrease shunt fraction, improve oxygenation and possibly
decrease pulmonary vascular resistance
Decreased venous return (ventricular preload) and LV wall tension (afterload)
Ventilation at higher lung volumes may overcome dynamic airflow obstruction and decrease
work-of breathing.
Over-distention with excessive lung volumes and/or pressures can contribute to ventilator
associated lung injury and injure other organs through humoral mediators. Over-distention can
also increase pulmonary vascular resistance and decrease cardiac output

III) Modes of Mechanical Ventilation

A) Continuous positive airway pressure (CPAP). The ventilator generates sufficient
airflow to maintain a constant column of pressure in the airway. The patients inspiratory
efforts create negative pleural pressure which drives air into alveoli. The patient expires
by creating positive pleural pressure which pushes air out the exhalation limb. Used
commonly via non-invasive ventilation to relieve obstruction in the treatment of sleep
apnea and to reduce preload/afterload in CHF.

Settings: CPAP pressure, FiO2
Variables: Respiratory rate, tidal volume, inspiratory flow rates and times

B) Assist Control (AC) volume cycled ventilation. The machine delivers a guaranteed
number of breaths each minute. The machine blows air into the inspiration limb at a set
rate up to a set tidal volume. The exhalation limb opens and air flows out of the lungs
until no gradient exists between the alveoli and the lower airway pressure you set
(PEEP). If the patient attempts additional breaths the machine will attempt to deliver the
full tidal volume if patient effort exceeds a set threshold.

You set: FiO2, PEEP, respiratory rate, inspiratory flow rate & pattern, tidal volume,
sensitivity to trigger inspiration
Variables: respiratory rate, exhaled tidal volume, peak airway pressure, inspiration and
exhalation times
C) AC Pressure Control- time cycled ventilation. The machine delivers a guaranteed
number of breaths each minute. The machine blows air into the inspiration limb at a rate
sufficient to generate a set pressure. The greater the patient (negative pressure) effort the
faster the vent has to push in air to maintain the airway pressure. Inspiration continues for
a set time interval. The ventilator then cycles over to exhalation and air flows out of the
lungs until the pressure falls to PEEP.

You set: FiO2, PEEP, respiratory rate, inspiratory time, inspiratory pressure, sensitivity to
trigger inspiration
Variables: respiratory rate, exhaled tidal volume, inspiratory flow

D) Pressure support-flow cycled ventilation (often erroneously called CPAP): No
guaranteed rate or tidal volume (i.e. no machine generated breaths). When patient
(negative) effort exceeds a threshold the machine pushes air into the inspiration limb with
force sufficient to generate the set pressure. The greater the patient (negative pressure)
effort the faster the vent has to push in air to maintain the airway pressure. Inspiration
continues until patient effort decreases enough that inspiratory flow rate falls below a set
threshold.

You set: FiO2, PEEP, pressure support, inspiratory and expiratory flow sensitivity
Variables: respiratory rate, exhaled tidal volume, peak airway pressure

E) Synchronized Intermittent Mandatory Ventilation (SIMV): The machine delivers a
guaranteed rate of volume cycled breaths. Additional spontaneously generated breaths
will be pressure support-flow cycled. Originally designed as a weaning mode, in clinical
trials this mode was inferior to once daily trials of spontaneous breathing.

III) Basic steps to Improve Oxygenation (measured by SaO2, PaO2)
A) Treat underlying pulmonary pathology (e.g. diurese pulmonary edema)
B) Increase FiO2
C) Increase Mean Airway Pressure (by increasing positive end expiratory pressure (PEEP)
or prolonging inspiratory time

IV) Basic Steps to Improve Ventilation (measured by minute ventilation, pH and PCO2)
A) Increase respiratory rate
B) Increase tidal volume (or increase pressure support on spontaneous breaths)

V) Causes of Common Ventilator Alarms
A) High Peak Airway Pressure (usually >36 cmH2O) caused by:
Decreased compliance (pneumonia, fibrosis, pulmonary edema, chest wall abnormalities,
ascites, tension pneumothorax, abdominal compartment syndromes)
Increased resistance to airflow (secretions, obstructed endotracheal tube, bronchospasm)-
manifested by gradient between peak inspiratory pressure and pressure measured at end-
inspiratory pause [Ppeak-Pplateau > 5cm H2O on AC-volume cycled ventilation.

Patient-ventilator asynchrony

B) Low Exhaled Tidal Volume
On volume cycled breaths: leak around ET tube cuff or in ventilator tubing, broncho-
pleural fistula, high pressure cutoff terminating breath before complete tidal volume
delivered, patient-ventilator asynchrony
On pressure supported breaths: inadequate patient effort or pressure support

C) Dysfunctional Oxygen Sensor
One of the AICU ventilators will alarm when the FiO2 is set <40% because it improperly
senses a low FiO2. Ignore this alarm, titrate FiO2 based on peripheral oxygen saturation.

VI) Weaning Strategies
There is probably no such thing as "weaning": patient will tolerate extubation or not
There is no proof that you can train respiratory muscles with exercise/rest
Your job is to treat all reversible medical problems (such as malnourishment) and quickly identify
patients capable of tolerating extubation
Protocol based daily interruption of continuous sedation, regardless of whether or not you are
planning to wean the patient that day, decreases time to extubation (NEJM 342; 2000: 1471-1477)
Protocol of daily trials of spontaneous ventilation is superior to strategies of slowly lowering
SIMV or pressure support (NEJM 332; 1995: 345-350)

AICU Protocol: If patient hemodynamically stable, adequate mental status, FiO2 requirement <45%,
PEEP < 5cmH2O, then perform daily trials of spontaneous ventilation (either on T-piece or spontaneous
mode with pressure support 5cmH2O).
Predictors of extubation failure: Rapid shallow breathing index (respiratory rate/tidal volume in liters)
>105 patient, hemodynamic instability or signs of distress.

*All ventilated patients should be given a daily sedation holiday in which sedative medications are
stopped in the morning so the patients mental status can be assessed regardless of whether or not they meet
criteria for spontaneous breathing trial.


VII) Mechanical Ventilation Strategy for ARDS

Use of low tidal volume (6cc/kg of ideal body weight) reduces mortality compared to use of traditional
tidal volumes (10-15cc/kg) [absolute risk reduction 8.8% NEJM 2000; 342: 1301-1306]

Increase PEEP to allow decrease of FIO2 to less toxic levels (<60).
Ventilator settings as studied by the ARDSNET group Adapted from NEJM 342; 2000:1471-1477.
Principles of Sedation in the Intensive Care Unit

I) Problems: Pain, agitation, anxiety, confusion
- Determine etiology of problem: e.g. dyspnea, drug withdrawal, fear, delirium, hypoglycemia, etc.

II) Treatments: Analgesia, hypnotics, anxiolytics, anti-psychotics
- Also repositioning, re-orientation, reassurance, adjustment of ventilator settings
- Not all patients on mechanical ventilation need sedation

III) Drug therapy should include:
- Induction: Rapidly achieve desired effect; in general requires bolus of short-acting agent (i.e. for rapid
onset)
- Maintenance of desired effect; in general requires constant infusion or intermittent dosing of longer acting
agents.

IV) Sedatives (especially intravenous agents) can cause life threatening respiratory depression.
- Do not administer sedatives to patients not on mechanical ventilation unless you are certain it will not
cause worsening respiratory failure or hemodynamic instability

V) Under-treatment of pain and over-sedation of mechanically ventilated patients are common ICU
problems

VI) In general, you should interrupt continuous sedation every day and allow the patient to awaken. This
prevents over-sedation and decreases the duration of mechanical ventilation

VII) Hypnotics and sedatives (such as benzodiazepines) can precipitate agitation in patients with delirium
(so called paradoxical response)

VIII) Frail, elderly and debilitated patients are much more sensitive to sedatives and the lowest possible
doses should be used. (You can always give more if the dose is ineffective)

IX) A combination of agents may be helpful (e.g. combining an opiate with a benzodiazepine)

Titrate sedative to objective endpoints using minimum effective dose. Order sedatives with a goal
RASS score.
Score Term Description
+4 Combative Overtly combative, violent, immediate danger to staff
+3 Very agitated Pulls or removes tube(s) or catheter(s); aggressive
+2 Agitated Frequent non-purposeful movement, fights ventilator
+1 Restless Anxious but movements not aggressive or vigorous
0 Alert & calm
-1 Drowsy Not fully alert, but has sustained awakening (eye opening/eye
contact) to voice (> 10 seconds)
-2 Light Sedation Briefly awakens with eye contact to voice (<10 seconds)
-3 Mod Sedation Movement or eye opening to voice (but no eye contact)
-4 Deep sedation No response to voice, but movement or eye opening to physical
Stimulation
-5 Unarousable No response to voice or physical stimulation

Sedative agents commonly used in the AICU

Benzodiazepines: Excellent hypnotics and anxiolytics, also causes useful amnesia (anterograde). NO
ANALGESIC PROPERTIES. Cause respiratory depression and mild hypotension. Elderly patients clear
benzodiazepines and their active metabolites more slowly.

Midazolam: Very short onset to and duration of effect.
o Indicated for short-term sedation (< 24 hrs)
o Useful for procedures and immediate treatment of agitation.
o IV bolus (1-2mg) q 3-5minutes to intubated patients to rapidly induce sedation.
o Active metabolites accumulate during continuous infusion causing prolonged sedation
o Re-bolus every time you increase drip rate to achieve desired effect more quickly.

Diazepam: Compared with midazolam it has a much longer time to onset and duration of action. It is
metabolized in the liver, its half-life is 30-60hrs, but it has active metabolite with a half-life of 100hrs
o Indicated for short-term sedation (>24hrs)
o Dose intermittently IV or PO to maintain sedation.
o Do not rapidly titrate up the infusion rate. If patient becomes agitated rebolus.

Analgesic Agents commonly used in the AICU.

Opiates:
Superlative analgesics; also cause sedation. All opiates cause respiratory depression, constipation, mild
hypotension, nausea, decreased GI motility, urinary retention, cardiovascular effects and muscle rigidity.

Morphine sulfate: Has a longer duration of action; use intermittent bolus
o Intravenous bolus of 1-4mg to rapidly induce analgesia and sedation.
o Morphine causes more severe hypotension by vasodilation than other opiates (because of histamine
release).
o Active metabolite may cause prolonged sedation in the presence of renal insufficiency.

Fentanyl: Most rapid onset and shortest duration, but may accumulate with repeated dosing
o Administer intravenous bolus to intubated patients (usually 50 mcg) up to q3minutes to rapidly induce
analgesia and mild sedation.
o Use continuous infusion for maintenance of analgesia, relief of dyspnea and mild sedation.
o If a patient on a fentanyl infusion becomes agitated consider repeated boluses of 2-4mg midazolam
injection. Lorazepam (1-2mg q 4-6 hours) can be used in addition to the fentanyl infusion for maintenance
of sedation.

Pethidine (Meperidine):
o Use with caution because of drug interactions and an eleptogenic active metabolite (normeperidine) that
accumulates in renal failure.

Agent Equianalge
sic Dose
(i.v.)
Half-life Duration
of Action
Active
Metabolite
s (Effect)
Adverse
Effects
Intermitte
nt Dose
Infusion
Dose
Range
Morphine 10 mg 3-7 hr 4 hrs
Yes (sedation,
especially in
renal
insufficiency)
Histamine
release
0.010.15
mg/kg IV q
12 hr
0.070.5
mg/kg/hr
Fentanyl 200
micrograms
1.5 6 hr 30 60
min
No metabolite,
parent
accumulates
Rigidity
with high
doses
0.351.5
microgram/
kg IV. q
0.51 hr
0.710
microgram/
kg/hr
Meperidine 75- 100 mg 3-4 hr 1 3 hrs
Yes
(neuroexcitati
on, especially
in
renal
insufficiency
or high doses)
Avoid with
MAOIs and
SSRIs
Not
recommend
ed
Not
recommend
ed

Paralytics: Neuromuscular blocking agents (NMBAs)
o These agents supply neither analgesia nor sedation.
o Used in ICU to:
o Manage ventilation
o Manage increased ICP
o Treat muscle spasms
o Decrease oxygen consumption
o They are only used in patients who are fully sedated to RASS -5 to facilitate either endotracheal
intubation by attending physicians or control of patients difficult to manage on mechanical ventilation.
o Used with extreme caution under direct supervision of AICU Specialist
o Cause complete apnea.
o Cause severe polyneuropathy (synergistic with aminoglycosides or corticosteroids).