Manual for Medical Students

7/27/2019 Manual for Medical Students

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Bugando Medical Center

Adult Intensive Care Unit

Resident and Student Manual

2011


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Part I: AICU Expectations

Introduction:

The Adult Intensive Care Unit (AICU) provides intensive medical management ofcritically ill patients at Bugando Medical Center. Patients admitted to the medical,

surgical and obstetrics/gynecology services can be cared for in the AICU. The MedicalICU 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 thruFriday 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 primarilyresponsible for their care. New patients should be picked up by a member of theteam. 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 theday 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 beavailable in the AICU at this time.

All patient notes, including impression and plan, should be written before AICUrounds with the specialist.

All notes written by students must be reviewed and countersigned by theresponsible resident in the AICU.

Residents and students are responsible for the completion of all components of theplan 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 anytests. Any adjustments can be made to the plan based on these assessments.

Formal afternoon rounds will occur at 4PM every afternoon with the AICUresidents and students together with the on-call medicine resident to review allpatients and make any necessary changes in plan.

For every patient that dies in the AICU, the family should be immediatelycontacted to request an autopsy.


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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 forgetimportant details of the patients progress or management.

Subjective1)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 areprescribing 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. Alsoreport type, amount and rate of IV fluid given in the last 24 hours remembering that IV fluids are

medications.

Assessment:

12)Impression: list the patientscurrent 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.


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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)


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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 youmake 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 thetime 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. Bedsideultrasound, 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 pericardialeffusion.

Localization of the kidneys and bladder. Assessment for hydronephrosis.

Assessment of pleural effusion.

Assessment of ascites.

Assessment of liver parenchyma.


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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 withforceps). 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 endotrachealintubation until adequate pre-oxygenation and ventilation have been performed. One of the most commonerrors 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 approximately2/3 of it lies within the mouth. Next, rotate the oral airway 180 0 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 overwhelmingmajority of patients


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- 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

ShockShock is a syndrome of acute circulatory failure associated with ineffective tissue perfusion andcellular injury.

Cellular injury manifests as multi-system organ dysfunction which is initially reversible. Persistent shockleads 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 oftheir 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 curveupward. 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 compliancediastolic dysfunction.


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The above graph is an idealized representation. Many doubt the presence of a decrease in SV fromventricular 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 transducingany 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 ofthe catheter measures the fall and recovery of the temperature of blood in the pulmonary artery. The areaunder 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


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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 + VO2Therefore:

Q = VO2/CaO2CvO2

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 thecardiac 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, alimiting 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 DO2

Urine Output SvO2

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 inthe 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 ismaintained 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


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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 perfusionOxygen 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 relativeextraction of delivered oxygen will maintain QO2. The mechanism of the increased extraction is likelyrelated 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 perfusionSvO2 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 fromblood 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 anormal 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 clinicalscenario 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 ofrespiratory 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


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pulmonary edema from endothelial dysfunction commonly cause severe hypoxia (ARDS).

Renal: oliguria ( 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, pericardialtamponade, 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 beelevated 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 exogenouscatecholamines (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,


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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 oftenelevated and the tissues are unable to utilize the delivered substrate.

Management Of Shock

1) Secure airway2) Guarantee adequate oxygenation and ventilation

3) Resuscitate circulationLarge bore IV access

CrystalloidMonitor adequacy of resuscitation

4) Continuous presence of trained clinician at bedside

5) Vasopressors if shock is refractory to fluids6) 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 saturationmonitoring, and most will require an arterial line. CVP monitoring is a flawed measure of fluidresponsiveness but indicated if patient is hemodynamically unstable.

Survival requires prompt and adequate fluid resuscitation. In general administer isotoniccrystalloid (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 venousblood (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


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20 gauge angiocath: maximum infusion rate: 60 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 areideal. Electric pumps willslow 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 bleedingbecause 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 CoagulopathyDecreased respiratory compliance Hypothermia

Pulmonary Edema Dilution of clotting factorsAbdominal compartment syndrome Hypocalcemia

Complications of Normal Saline Complications of PRBC

Metabolic acidosis Viral infection (very rare)Hypernatremia Nosocomial PneumoniaHypokalemia

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. Othertherapies 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 inpatients in shock.


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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:Dopaminedose responses for various receptors vary;

1-3 mcg/kg/min dopaminergic receptors predominate with dilation of renal and splanchnic vessels. Somevasodilatation 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]

EpinephrineAt 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 increasingvasoconstriction and BP. Epinephrine is the drug of choice for anaphylaxis.

DobutaminePotent 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 patienttolerates 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 inhypotensive patients.

Other Important Vasopressors not currently available at BMCNorepinephrine (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.

VasopressinUsed 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.


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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 whichdrives 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 patientsairways. 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 possiblydecrease pulmonary vascular resistance

Decreased venous return (ventricular preload) and LV wall tension (afterload)

Ventilation at higher lung volumes may overcome dynamic airflow obstruction and decreasework-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 sleepapnea and to reduce preload/afterload in CHF.

Settings: CPAP pressure, FiO2Variables: 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 ratesufficient 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


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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 setthreshold.

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 AlarmsA) 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


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AICU Protocol:If patient hemodynamically stable, adequate mental status, FiO2 requirement 105 patient, hemodynamic instability or signs of distress.

*All ventilatedpatients 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 (


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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 ICUproblems

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/eyecontact) to voice (> 10 seconds)

-2 Light Sedation Briefly awakens with eye contact to voice (


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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 boluso 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 inrenal

insufficiency)

Histaminerelease

0.010.15mg/kg IV q

12 hr

0.070.5mg/kg/hr

Fentanyl 200

micrograms

1.56 hr 3060

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 13 hrs Yes(neuroexcitati

on, especially

inrenalinsufficiency

or high doses)

Avoid withMAOIs andSSRIs

Notrecommended

Notrecommended


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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 consumptiono 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).

Manual for Medical Students

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