Chapter 66: Nursing Management Critical Care

Critical Care Nursing

Critical Care/Intensive Care Units
PICU any type of pediatric intensive care patient except cardiac
NICU infant that has to have never left the hospital
Critical Care Nurse
o Performs frequent assessments to monitor trends in patients physiologic
parameters (BP, ECG, etc.)
o Provides psychologic support to patient and caregiver(s)
o Important to be skilled in palliative and end-of-life care
o Certifications critical care nurses can get
Critical Care Certification (CCRN)
Progressive Care Certification (PCCN)
Cardiac Medicine (CMC)
Cardiac Surgery (CSC)
o Nurses should be aware of the scope of practice provided by their state's Nurse
Practice Act
In general, nurses can provide
Patient and caregiver teaching about an illness or disease
The general course of illness
What usual treatment entails
Diagnosis and prognosis are outside the scope of practice for a
registered nurse
Critical Care Patient
o Common Problems of Critical Care Patients
Usually immobile and at high risk for thromboembolism and skin
problems
Use of multiple invasive devices predisposes patient to hospital-acquired
infections
Sepsis and multiple organ dysfunction (MODS) may follow
Nutrition
Must collaborate with physician and dietician to determine how
to meet nutritional needs
Primary goal is to prevent or correct nutritional deficiencies
Usually accomplished with Enteral (calories via GI tract) and
Parenteral (calories via IV) nutrition
Enteral nutrition is usually encouraged
Preserves the structure and function of the gut mucosa
Prevents the movement of gut bacteria across the
intestinal wall and into the bloodstream
In addition, early enteral nutrition is associated with
fewer complications and shorter hospital stays, and is
less expensive than parenteral nutrition
Parenteral nutrition is used when Enteral route is unsuccessful or
contraindicated
Paralytic ileus, diffuse peritonitis, intestinal obstruction,
pancreatitis, GI ischemia, intractable vomiting, and
severe diarrhea

Anxiety
Encourage patients and caregivers to express concerns, ask
questions, and state their needs
Include patient & caregiver in all conversations and explain
purpose of equipment & procedures
Structure patient's surrounding environment in a way that
decreases anxiety
For example, encourage caregivers to bring in
photographs and personal items
Judicious use of antianxiety drugs (e.g., lorazepam [Ativan]) and
complementary therapies (e.g., guided imagery, massage) may
reduce stress response that can be triggered by anxiety
Pain
Control of pain is paramount as many as 70% in ICU have
moderate to severe uncontrolled pain
ICU patients at high risk for pain include patients who
Have medical conditions that include ischemic,
infectious, or inflammatory processes
Are immobilized
Have invasive monitoring devices, including
endotracheal tubes
Require invasive or noninvasive procedures
If giving Propofol for sedation, a daily sedation vacation
(interruption of sedation) should be conducted allows patient to
wake so a neurological assessment can be done
Patients who are intubated can feel pain (could be grimacing or
show change in vitals)
If doing a dressing change, should give them prophylactic pain
meds
Impaired communication
Some patients may not be able to speak b/c of the use of sedative
and paralyzing drugs or an endotracheal tube
Always explain what will happen or is happening to the patient
when doing any procedure
Explore using picture boards, notepads, magic slates, or
computer keyboards if they cant talk
Look directly at patient when speaking to them and use gestures
when appropriate
Comfort touch is important to some patients
Encourage caregivers to touch and talk with the patient
even if patient is unresponsive or comatose
Sensory-Perceptual Problems
Estimated that the prevalence of delirium in ICU patients is as
high as 80%
Factors Predisposing Patient to Delirium
Demographic factors advanced age, preexisting
cognitive impairment, vision/hearing impairments,
history of drug or alcohol abuse

Environmental factors sleep deprivation, anxiety,

sensory overload, immobilization
Physical conditions hemodynamic instability,
hypoxemia, hypercarbia, electrolyte disturbances, severe
infections
Certain drugs sedatives, Lasix, antimicrobials
Must address physiologic factors (e.g. correct O2 levels,
perfusion, and electrolyte problems)
Use of clocks and calendars can help orient patient
Presence of caregiver may help orient patient and reduce
agitation
Neuroleptic drugs (Haldol) can be used if patient demonstrates
hyperactivity, insomnia, delusions
Limit noise and explain noises that cannot be prevented
Have conversations out of patient area unless involving
patient in conversation
Silent unnecessary alarms while doing procedures then
reactivate them when done
Sleep Problems
Nearly all patients in ICU experience sleep disturbances
significant stressor in ICU
Contributes to delirium and possibly affects recovery
Structure environment to promote patients sleep-wake cycle
Cluster activities
Schedule rest periods
Dim lights at nighttime
Open curtains during the daytime
Obtain physiologic measurements w/o disturbing patient
Limit noise
Provide comfort measures (e.g. back rubs)
Many patients on sleep aids to induce/maintain sleep benzos
(Restoril) & benzo-like (Ambien)
Issues Related to Caregivers
o To be effective in caring for their loved one, caregivers need your guidance and
support
o Caregivers experience anxiety regarding patients condition, prognosis, pain and
other discomforts, and finances
If anxious about finances, consulting with case manager or social worker
is helpful
o Nurses must provide family-centered care need skills in crisis intervention
Interventions active listening, reduction of anxiety, support of those
who become upset or angry, acknowledgment of caregivers feelings and
acceptance of their decisions, meeting informational, reassurance, and
convenience needs
Note: patients often exhibit early and subtle signs of deterioration (e.g. mild confusion,
tachycardia) 6-8 hours before cardiac and/or respiratory arrest

Drugs Related to Critical Care

Dopamine
o Increases contractility of the heart CO is increased
o Renal dose will open up the kidney function and helps increase urine output
o At higher levels, blood pressure is increased and renal perfusion is decreased
Dobutamine
o Helps the heart pump efficiently
o Use in cardiogenic shock
Levophed
o Vasoconstriction, which helps increase blood pressure
o Long-term use can cause necrosis of the extremities fingers, toes, etc.
Nitroglycerin
o Vasodilation, which relieves chest pain
o Can give the patient a severe headache usually will give them Tylenol as well
Propofol
o Sedation
o Also helps for nausea leaves the body very quickly so it does not help the
nausea for long
o Can drop BP quickly
o Two Types
Regular
Nut based watch for nut allergies to avoid anaphylaxis
Prescedex
o Sedation
Epinephrine
o Low BP, allergic reaction
Norepenephrine/Levophed
o Shunt the blood to vital organ extremities are effected the most
Amiodorone
o Antidysmic

Hemodynamic Monitoring
Measurement of pressure, flow, and oxygenation within the cardiovascular system
o Invasive monitoring internally placed devices
o Noninvasive monitoring external devices
Values Commonly Measured in the ICU
o Systemic and pulmonary arterial pressures
o Central venous pressure (CVP)
o Pulmonary artery wedge pressure (PAWP) (also known as pulmonary artery
occlusive pressure [PAOP])
o CO/CI
o SV/SV index [SVI]
o O2 saturation of the hemoglobin of arterial blood (SaO2)
o Mixed venous oxygen saturation (SvO2)
o These measurements allow you to calculate
Resistance of the systemic and pulmonary arterial vasculature
O2 content, delivery, and consumption
Hemodynamic Terminology

o
o
o
o

o
o
o

Cardiac Output volume of blood in liters pumped by the heart in 1 minute

Cardiac Index measurement of CO adjusted for body surface area (BSA)
More precise measurement of the efficiency of the pumping action of the
heart
Preload volume in ventricle at the end of diastole
Afterload forces opposing ventricular ejection
Systemic arterial pressure, resistance by aortic valve, and mass and
density of the blood to be moved
WANT TO LOOK AT SVR IN REGARDS TO AFTERLOAD (systemic
vascular resistance)
Systemic Vascular Resistance resistance of the systemic vascular bed
Pulmonary Vascular Resistance resistance of the pulmonary vascular bed
Contractility strength of the contraction
If preload, heart rate, and afterload remain constant yet CO changes,
contractility is changed
Contractility is reduced in the failing heart

Principles of Invasive Pressure Monitoring

o Invasive lines used in the ICU to measure systemic and pulmonary BPs
o Pressure monitoring equipment is referenced and zero balanced to the
environment
Referencing positioning transducer so the zero reference point is at the
level of the atria of the heart
Stopcock nearest transducer usually the zero reference for the
transducer
To place this level with atria, need to find phlebostatic axis

Transducers placed higher than the phlebostatic axis will

produce falsely low readings
Transducers placed lower than the phlebostatic axis will produce
falsely high readings
Zeroing confirms that when pressure within the system is zero, the
monitor reads zero
Open reference stopcock to room air (off the patient) and watch
for a reading of zero
This allows use of atmospheric pressure as a reference for zero
When to Zero?
During the initial setup
Immediately after insertion of arterial line when
transducer has been disconnected from pressure cable or
pressure cable has been disconnected from monitor
When the accuracy of the measurements is questioned
Types of Invasive Pressure Monitoring
o Arterial Blood Pressure 20 gauge in the radial or femoral artery sutured in
place
Measurement of Blood Pressure with Invasive Lines
Radial, brachial, or femoral
Want to watch for infection red, swollen
Should have good wave form and be zeroed (check zero to the
transducer at the 4th intercostal space)
Cuff pressure should be within 10 of arterial pressure
Complications
Hemorrhage use Luer-Lok connections, check arterial
waveforms, and activate alarms
If pressure in line falls (when line disconnects) an alarm
will sound
Infection inspect insertion site for inflammation/infection
Change pressure tubing, flush bag, and transducer q96h
When infection is suspected, remove catheter and
replace equipment
Thrombus formation
To limit thrombus formation and maintain line patency,
check continuous flush system q1-4h to make sure the
pressure bag is inflated to 300 mm Hg, the flush bag
contains fluid, and the system is delivering 3-6 mL/hour
Should not be using heparin routinely for flush solution
risk for thrombocytopenia
Neurovascular impairment
Loss of limb

Pulmonary Artery Flow-Directed Catheter

Pulmonary Artery Catheter Insertion
Note patients electrolyte, acid-base, oxygenation, and
coagulation status

 Imbalances such as hypokalemia, hypomagnesemia, hypoxemia,

or acidosis can make heart more irritable & increase risk of
ventricular dysrhythmia during catheter insertion
To maintain position, catheter is secured at point of entry on skin
and length marked

Pulmonary Artery Pressure Measurements

PAD (pulmonary artery diastolic pressure) & PAWP (pulmonary
artery wedge pressure)
Both are sensitive indicators of cardiac function and
fluid volume status
Both increase in heart failure and fluid volume overload
Both with volume depletion
PAWP is pressure generated by left ventricle (left
ventricle function)
Basing fluid therapy on PA pressure can restore fluid balance
w/o overcorrection or undercorrection of the problem (can avoid
pulmonary edema)
Complications with Pulmonary Artery Catheters
Infection and Sepsis
Must have careful surgical asepsis for insertion and
maintenance of catheter & tubing
Monitor patient for local and systemic changes
redness, exudate at insertion site, fever, increased WBC
count
Must remove catheter if there are any signs of infection
To reduce risk of infection change flush bag, pressure
tubing, & stopcock q96h and remove hemodynamic
monitoring once it is no longer needed

Air Embolus
Always check balloon integrity before insertion
discard defective catheters
After insertion, balloon rupture or injection of air into
any lumen can cause air embolus
To reduce risk of air embolus first aspirate blood to
check for absence or presence of blood and only inject
prescribed volume of air into balloon before obtaining
PAWP
o If blood is aspirated from balloon port or balloon
air does not all come back into the syringe, label
port do not use and contact physician
Always use Luer-Loks on all pressure lines and activate
low pressure alarms
Pulmonary Infarction or PA Rupture
Causes
o Balloon may rupture, releasing air and
fragments that could embolize
o Prolonged balloon inflation may obstruct blood
flow
o Catheter may advance into a wedge position,
obstructing blood flow
o Thrombus could form and embolize
To reduce risk of air embolus/pulmonary infarction
never inflate balloon beyond capacity (1-1.5 mL of air),
monitor PA pressure waveforms continuously for
evidence of catheter occlusion, dislocation, or
spontaneous wedging
o Pressure tracing will be blunted with occlusion
and will appear wedged if PA catheter advances
and becomes wedged
o Physician must reposition catheter immediately
o ALWAYS CLOSE LINE WITH CLAMP OR
STOPCOCK WHEN LINE IS
DISCONNECTED
o NEVER LEAVE BALLOON INFLATED FOR
MORE THAN 4 BREATHS (8-15 SECONDS)
EXCEPT DURING INSERTION
To reduce risk of thrombus/embolus formation PA
catheter needs to be continuously flushed with a slow
infusion of normal saline
Ventricular Dysrhythmias
Can occur during PA catheter insertion or removal or if
tip moves from PA to R ventricle and irritates ventricular
wall (PA catheter would not be able to be wedged)
Needs to be repositioned by physician and chest x-ray
done to confirm location
Central Venous or Right Atrial Pressure Measurement (CVP)

Measurement of right ventricular preload

Measured with PA catheter using the proximal lumen located in the right
atrium or with a central venous catheter placed in the internal jugular or
subclavian vein
Also reflects fluid volume problems, but PA diastolic pressure & PAWP
are better indicators of it
Increase in CVP reflects heart failure or volume overload WANT TO
CVP TO CARDIAC OUPUT!!!
Decrease in CVP reflects volume depletion
CVP Waveform Interpretation
a wave represents atrial contraction
x descent represents atrial relaxation
c wave represents the bulging of the closed tricuspid valve into
the right atrium during ventricular systole
v wave represents atrial filling
y descent represents opening of the tricuspid valve and filling
of the ventricle

Invasive Cardiac Output Measurement Techniques

Normal resting cardiac output is 4-8L per minute
CO & CI are in shock states (e.g. cardiogenic, hypovolemic) and heart
failure
CO with exercise and at rest with fever or early sepsis
TDCO (intermittent bolus thermodilution CO)
CO is calculated from temperature change in pulmonary artery
when a fixed volume and known temperature of a solution is
injected into proximal port in right atrium
CO measured by computer from area under the temp curve
Want curve to be smooth
Larger area under curve = lower CO
Smaller area under curve = higher CO
Repeat 3x with each measurement 1-2 minutes apart to
determine CO
Must have three normal curves to be valid throw out
any abnormal curves
CCO (continuous cardiac output method)

CO measured with a PA catheter (placed in the right atrium) that

has a heat-exchange CO catheter attached to detect changes in
temp when blood passes through R ventricle
Every 30-60 seconds, a bedside computer displays average CO
for the past 3-6 minutes
Eliminates need for fluid boluses, decreases contamination,
permits ongoing evaluation
MORE RELIABLE THAN TDCO METHOD
Minimally Invasive Cardiac Output Monitoring Techniques
Use of a specialized sensor that attaches to a standard arterial pressure
line and a monitor
Measures CCO/CCI, SV/SVI, and stroke volume variation q20secs
More research needed to find if this approach can replace hemodynamic
monitoring with PA catheter
Venous Oxygen Saturation
Both CVP (central venous pressure) and PA (pulmonary artery) catheters
can include sensors to measure O2 saturation of hemoglobin in venous
blood
O2 saturation of blood from PA catheter = mixed venous oxygen
saturation (SvO)
O2 saturation of blood from CVP catheter = central venous
oxygen saturation (ScvO)
Both are adequate for the measurement of adequate tissue
oxygenation
Normal SvO/ScvO at rest is 60-80%
SvO/ScvO
arterial oxygenation, low CO, low hemoglobin,
consumption or extraction of O
If below 60%, observe for changes in arterial
oxygenation
o Monitor pulse oximetry or ABGs
o Indirectly assess CO and tissue perfusion
changes in mental status, strength or quality of
peripheral pulses, capillary refill, urine output,
skin color & temp
o If arterial oxygenation, CO, and hemoglobin are
unchanged, the in SvO/ScvO is from O
consumption or extraction could be
metabolic rate, pain, movement, or fever
SvO/ScvO
Could be from an improvement (e.g. O saturation,
improved perfusion, metabolic rate) or from a problem
(e.g. sepsis)
o In sepsis there is a ability of tissues to use O
at the cellular level

Noninvasive Hemodynamic Monitoring Impedance Cardiography (ICG)

o Method of obtaining CO and assessing thoracic fluid status continuous or
intermittent
o Uses four external electrodes that deliver a high frequency, low amplitude current
to measure the change in impedance in the ascending aorta and left ventricle over
time
Impedance the resistance to the flow of electric current
o Cannot use in patients with generalized edema or third spacing excess volume
interferes with accuracy
Noninvasive Arterial Oxygenation Monitoring Pulse Oximetry
o Monitoring SpO may reduce frequency of ABG sampling
o SpO is normally 95%-100%
o Can put pulse ox probe on forehead, earlobe, etc. if cannot get good reading on
fingers
o Normally used to evaluate effectiveness of oxygen therapy and how patient
tolerates position changes or decreases in fraction of inspired air (FIO)
Nursing Management of a Patient on Hemodynamic Monitoring
Obtain Baseline Data
o General appearance
Does the patient appear tired, weak, exhausted?
o Level of consciousness
Cardiac reserve may be insufficient to sustain even minimum activity
Changes in mental clarity may reflect problems with cerebral perfusion
or oxygenation
o Skin color/temperature
Pallor, cool skin, and diminished pulses may indicate decreased CO
If patient is bleeding and developing shock, BP might initially be stable,
yet patient may become increasingly pale and cool from peripheral
vasoconstriction
Conversely, patient with septic shock may remain warm/pink yet
develops tachycardia and BP instability
o Vital signs
o Peripheral pulses

Capillary Refill
Urine output
Monitoring urine output reflects the adequacy of perfusion to the kidneys
Patient with diminished perfusion to GI tract may have hypoactive or
absent bowel sounds
Correlate baseline data with data obtained from biotechnology
o e.g., ECG; arterial, CVP, PA, and PAWP pressures; SvO2/ScvO2
o Single hemodynamic values are rarely significant
o Monitor the whole clinical picture
o
o

Circulatory Assist Devices (CADs)

Used to decrease cardiac work & improve organ perfusion in patients with heart failure
when drugs are no longer adequate
All CADs decrease ventricular workload, increase myocardial perfusion, and augment
circulation
Provide Interim Support in Three Types of Situations
o Left, right, or both ventricles require support while recovering from acute injury
(e.g., postcardiotomy)
o Patient must be stabilized before surgical repair of the heart (e.g., a ruptured
septum)
o Heart has failed, and the patient is awaiting cardiac transplantation
Intraaortic Balloon Pump (IABP) most commonly used CAD
o Provides temporary circulatory assistance (improving coronary blood flow) to
compromised heart by
Reducing afterload (reducing systolic pressure)
Enhancing the aortic diastolic pressure

o
o

Balloon inserted percutaneously or surgically into the femoral artery, advanced

toward the heart, and positioned in the descending thoracic aorta just below the
left subclavian artery and above the renal arteries
During systole balloon is deflated (on R wave), which facilitates ejection
of the blood into the periphery
In early diastole, balloon begins to inflate (on T wave)
In late diastole, balloon is totally inflated
Increases aortic pressure and increases coronary perfusion
pressure with the end result of increased coronary and cerebral
blood flow
X-ray is used to verify location after placement
IABP therapy is called Counterpulsation balloon inflation is opposite to
ventricular contraction
1:1 ratio in acute phase of treatment one IABP cycle of inflation and
deflation for every heartbeat

Complications with IABP Therapy

Signs of a leak include
Less effective augmentation
Repeated alarms for gas loss
Blood backing up into the catheter
Patient is relatively immobile, limited to side-lying or supine positions
with HOB <45 degrees
May be difficult to find comfortable position
Patient may experience sleeplessness and anxiety
Adequate sedation, pain relief, skin care, and comfort measures
are essential
Nursing Considerations for Patient with IABP Therapy
Must perform frequent and thorough cardiovascular assessments that
include
o Measurement of hemodynamic parameters (e.g., PA and arterial
pressures, CO, CI, SVR, SV)
o Auscultation of the heart and lungs
o Evaluation of the ECG (e.g., rate, rhythm)
o Assess adequate tissue perfusion (e.g., skin color and
temperature, mental status, capillary refill, peripheral pulses,
urine output, bowel sounds) at regular intervals
o It is expected that IABP therapy will improve these
parameters
IABP therapy is weaned as patient improves 1:1 to 1:2 to 1:3, etc. until
line is removed/patient is stable
Pumping is continued until line is removed, even if patient is stable, to
avoid thrombus formation around catheter

Ventricular Assist Devices (VADs)

o Short and long-term support for the failing heart increase or replace action of
the ventricle
Temporary device with capability to partially or totally support
circulation until the heart recovers or a donor heart can be obtained
o Allows more mobility than the IABP
o Can be internal (e.g. peritoneum) or external
o Typically, shunts blood from left atrium or ventricle to the device, then to the
aorta some right or biventricular

Indications for VAD

Failure to wean from CPB (cardiopulmonary bypass) or postcardiotomy
cardiogenic shock
CPB technique that temporarily takes over the function of the
heart and lungs during surgery, maintaining the circulation of
blood and the oxygen content of the body
Cardiotomy cardiogenic shock heart has been damaged by an
incision made in the heart (sometimes used for suction during
heart surgery) and cannot supply enough blood to the body
Bridge to recovery or cardiac transplantation
Patients with New York Heart Association Classification IV who have
failed medical therapy
o Contraindications for VAD
BSA less than manufacturer's limit (e.g., 1.3 m2)
Renal or liver failure unrelated to a cardiac event
Co-morbidities that would limit life expectancy to less than 3 years
o Nursing Considerations for Patient with a VAD
Similar to that of the patient with an IABP
Observe the patient for bleeding, cardiac tamponade, ventricular failure,
infection, dysrhythmias, renal failure, hemolysis, and thromboembolism
Unlike patient with an IABP, who must remain in bed with limited
position change, patient with VAD may be mobile and requires an
activity plan
In some cases, patients with VADs may go home
Preparation for discharge is complex and requires in-depth
teaching about the device and support equipment (e.g., battery
chargers)
Patients must have a competent caregiver present at all times
Implantable Artificial Heart
o Used to replace the heart of patients who are not eligible for a transplant and
have no other treatment alternative
o Less expensive implantation and drug therapies than an organ transplant
Patients do not require immunosuppression therapy & dont experience
long-term effects of this therapy
o PATIENTS REQUIRE LIFELONG ANTICOAGULATION THERAPY
Nursing Management for All Circulatory Assist Devices (IABP & VAD)
Goal is recovery through
o Ventricular improvement
o Heart transplantation
o Artificial heart implantation
Many patients will die or choose to terminate device, causing death
Psychologic support for patient and caregiver is essential
Artificial Airways
Endotracheal Tube Intubation
o Tube is placed into the trachea via the mouth or nose past the larynx
o Performed quickly and safely at the bedside
o Oral Intubation
o

ET tube passed through mouth and vocal cords into trachea with aid of a
laryngoscope or bronchoscope

Oral intubation preferred for most emergencies b/c airway can be secured
rapidly
Uses a larger-diameter tube than nasal route, which reduces the work of
breathing (WOB) due to less airway resistance
Risks of Oral Intubation
May be difficult to place if head and neck mobility is limited
(e.g. suspected spinal cord injury)
Teeth can be chipped or dislodged during procedure
Salivation is increased and swallowing is difficult
Patient may obstruct ET tube by biting down on it
o Can use sedation along with bite block or oropharnygeal
airway to avoid this
Mouth care is a challenge due to limited space in oral cavity
o Can use smaller/pediatric-sized oral products for tooth
brushing, cleaning, & suctioning
Nasal Intubation
ET tube is placed blindly (without seeing larynx) through the nose,
nasopharynx, and vocal cords
Nasal intubation used when head and neck manipulation is risky

Contraindications for Nasal Intubation

Patients with facial fractures
Suspected fractures at the base of the skull
Postoperatively after cranial surgeries

Downfalls of Nasal Intubation

Nasal tube uncomfortable for some because it presses on the
septum
o Some do prefer nasal though b/c no need for bite block
and mouth care is easier
More subject to kinking than oral tubes
WOB is greater due to longer, narrower tubes that have more
airflow resistance
Suctioning and secretion removal are more difficult
Linked with sinus infection and ventilator-associated pneumonia
o Indications for Endotracheal Intubation
Upper airway obstruction (e.g., secondary to burns, tumor, bleeding)
Apnea
High risk of aspiration
Ineffective clearance of secretions
Respiratory distress
Tracheostomy
o Surgical procedure that is performed when the need for an artificial airway is
expected to be long term
o Early tracheostomy (2-10 days) may have advantages over delayed, particularly
when need for mechanical ventilation is predicted to be longer than 10-14 days
Endotracheal Intubation Procedure
o Unless emergent, consent for procedure is needed
o Important to tell patient
they will not be able to speak during intubation but you will provide
other means of communication
their hands may be restrained for safety purposes
o Required for Intubation/Mechanical Ventilation
Self-inflating bag-valve-mask (BVM) available & attached to O
Ambu bag
The slower the bag is deflated/inflated, the higher the O
concentration (90-95% from reservoir)
Suctioning equipment ready at bedside
IV access
o Before Intubation
Assemble and check the equipment to be used
Remove patients dentures and/or partial plates (for oral intubation)
Administer drugs as ordered
Preoxygenate the patient using Ambu bag and 100% O for 3-5 minutes
Ventilate b/w each attempt using Ambu bag and 100% O
EACH ATTEMPT IS LIMITED TO < 30 SECONDS
For oral intubation, place patient supine with the head extended and neck
flexed (sniffing position)
Allows visualization of vocal cords by aligning axes of mouth,
pharynx, and trachea
o After Intubation
Inflate the cuff and confirm placement of ET tube while patient is
manually ventilated

Once x-ray confirms proper placement, mark position of tube at lip, teeth
or nose
Obtain ABGs within 25 minutes after intubation to get oxygenation and
ventilation status
Continue pulse ox monitoring to estimate arterial oxygenation
IF PATIENT PULLS TUBE OUT, BAG THEM IMMEDIATELY
Rapid-sequence intubation (RSI)
Rapid, concurrent administration of both a paralytic and a sedative agent
during emergency airway management to decrease risk of aspiration,
combativeness, and injury to patient
NOT INDICATED IN PATIENTS WHO ARE COMATOSE OR IN
CARDIAC ARREST
Must monitor patients O status during procedure with pulse ox
Medications Often Used

Use an end-tidal CO detector to measure the amount of exhaled

CO from lungs
Place detector b/w Ambu bag and ET tube if there is a color
change, CO is present
If no CO detected, tube is in esophagus and needs to be
reinserted
CO Detector is MOST ACCURATE way to determine if tube is
in lungs
Auscultate lung apices/bases for bilateral breath sounds
Listen for lung sounds if CO detector is not available
Auscultate epigastrium to check for absence of air insufflations
Observe chest for symmetric chest wall movement
SpO should be stable or improved look at patients color as well
After all evidence above shows proper placement, connect tube to O
source and secure
ET tube connected to either humidified air, O, or a mechanical
ventilator
Suction ET tube and pharynx
Insert bite block as needed
Arrange for portable chest x-ray immediately to confirm tube location (35 cm above carina in adult)
Allows patient to move neck w/o dislodging tube or causing it to
enter right primary bronchus

 Sedative-hypnotic amnesic (midazolam [Versed]) if agitated,

disoriented, combative
Rapid-onset opioid (fentanyl [Sublimaze]) to blunt pain of
laryngoscopy and intubation
Paralytic drug (succinylcholine [Anectine]) to produce skeletal
muscle paralysis
Atropine to limit secretions
Nursing Management for Artificial Airways
Maintaining Correct Tube Placement
o Monitor ET tube placement every 2-4 hours
o Confirm exit mark on ET tube remains constant while
At rest
Providing patient care
Repositioning
Transporting
o Incorrect tube placement is an emergency
Stay with patient and maintain airway
Support ventilation
Secure help immediately
If necessary, ventilate with BVM and 100% O
o If dislodged tube isnt repositioned, minimal or no O2 is delivered to lungs or
entire tidal volume is delivered to one lung places the patient at risk for
pneumothorax
Maintaining Proper Cuff Inflation
o Cuff is an inflatable, pliable sleeve encircling outer wall of ET tube
o Stabilizes and seals ET tube within trachea and prevents escape of ventilating
gases
o Cuff can cause tracheal damage
o Measures to Avoid Tracheal Damage by Cuff
Inflate the cuff with air measure & monitor cuff pressure
Normal arterial tracheal perfusion is estimated at 30 mm Hg
Cuff pressure should be maintained at 20 to 25 mm Hg
Cuff pressure is measured and recorded after intubation and on a routine
basis (q8h) using
Minimal occluding volume technique (MOV)
Mechanically Ventilated Patients
o Place stethoscope over trachea
o Inflate cuff to MOV by adding air until no air
leak heard at peak inspiratory pressure
Spontaneously Breathing Patients
o Inflate cuff until no sound heard after deep
breath or after inhalation w/ a BVM
o Use manometer to verify cuff pressure is
between 20 and 25 mm Hg
o Record cuff pressure in chart
If adequate cuff pressure cannot be maintained, or larger
volumes of air are needed to keep the cuff inflated, the

cuff could be leaking, or tracheal dilation could occur at

the cuff site
o In this situation, notify physician to reposition or
change the ET tube
Minimal leak technique (MLT)
Similar to MOV, except you remove small amount of air
from cuff until a slight air leak is auscultated at peak
inflation
Both techniques aim to prevent risks of tracheal damage due to
high cuff pressures
Monitoring Oxygenation and Ventilation
o Auscultate to confirm bilateral breath sounds
o Monitor patient for adequate oxygenation by assessing clinical findings ABGs,
SpO2, and SvO2/ScvO2
o Assess for signs of hypoxemia change in mental status (e.g., confusion),
anxiety, dusky skin & dysrhythmias
Maintaining Tube Patency
o You should NOT routinely suction a patient must assess first to determine need
for suctioning
o Indications for Suctioning
Visible secretions in the ET tube
Sudden onset of respiratory distress
Suspected aspiration of secretions
Increase in peak airway pressures
Auscultation of adventitious breath sounds over the trachea and/or
bronchi
Increase in respiratory rate and/or sustained coughing
Sudden or gradual decrease in PaO and/or SpO
o Open Suction Technique (OST) or Closed Suction Technique (CST)
CST maintains oxygenation and ventilation during suction and reduces
exposure to patients secretions
o Prevent hypoxemia by hyperventilating patient before beginning & between each
pass with Ambu bag & 100% O and limiting each pass to 10 seconds or less
o Keep suction pressure under 120 mmHg to avoid damage to the tracheal mucosa
increases risk of infection
o Make sure to adequately hydrate patient and humidify inspired gases to thin
secretions if too thick to suction
o Try postural drainage, percussion and turning patient q2h to help move secretions
into larger airways
Providing Oral Care and Maintaining Skin Integrity
o Use saline or water swabs to prevent mucosal drying (lips, tongue, gums)
o Reposition and retape ET tube q24h and as needed to avoid skin breakdown from
pressure of tubing

Fostering Comfort and Communication

o Patients may experience anxiety related to inability to communicate well and not
knowing what to expect
o ET tube often requires sedating the patient until it is no longer required to blunt
anxiety and discomfort
Complications of Endotracheal Intubation
o Unplanned (inadvertent) Extubation
Unplanned removal of the ET tube from the trachea can be catastrophic
& usually complicates recovery
Can be due to patient removal or accidental removal from movement or
procedures
Can be obvious (patient holding tube) or not so obvious (tip of tube in
hypopharynx or esophagus)
Signs of Unplanned Extubation
Patient speaking
Activation of the low-pressure ventilator alarm
Diminished or absent breath sounds
Respiratory distress
Gastric distention
Should this occur, remain with patient, call for help, and manually
ventilate with Ambu bag at 100% O
o Aspiration
Airway not protected from aspiration due to tube splinting epiglottis in
open position
Cuff cannot totally prevent trickle or oral/gastric secretions from entering
trachea
Secretions accumulate above the cuff and when it is deflated, those
secretions can move into the lungs

 Some ET tubes provide continuous suctioning of secretions

above the cuff
Oral intubation causes an increase in salivation and difficulty swallowing
must suction when needed
All intubated patients receiving enteral feedings must have HOB
elevated a minimum of 30-35 degrees unless medically contraindicated
Mechanical Ventilation
FIO is at 21% (room air) or greater and is moved in and out of lungs by a mechanical
ventilator
Mechanical ventilation is NOT curative
o Supports patients until able to independently breath or until a decision is made to
withdraw mechanical ventilation
Negative Pressure Ventilation
o Encases the chest and uses negative pressure to pull the chest outward reduces
intrathoracic pressure
o Air rushes into the upper airway, which is outside the sealed chamber
o Expiration is passive machine cycles off to allow chest to retract
o Noninvasive does not require artificial airway
Positive Pressure Ventilation
o Volume ventilation predetermined tidal volume is delivered with each
inspiration
o Pressure ventilation peak inspiratory volume is predetermined
Settings of Mechanical Ventilation

Mechanical Ventilation Alarms and What Causes and Activation

Complications of Positive Pressure Ventilation

o Cardiovascular System
o Pulmonary system
Barotrauma
Volutrauma
Alveolar hypoventilation
Alveolar hyperventilation
Ventilator-associated pneumonia
o Sodium and water imbalance
o Neurologic system
o Gastrointestinal system
o Musculoskeletal system
o Psychosocial needs
o Machine disconnection or malfunction

Chapter 67: Shock/SIRS/MODS (10 questions)

What is Shock?
Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism
Imbalance in supply/demand for O2 and nutrients
Types of Shock
Cardiogenic Shock
o Systolic or diastolic dysfunction
o Compromised cardiac output (CO)
o Precipitating Causes
Myocardial infarction
Cardiomyopathy
Blunt cardiac injury
Severe systemic or pulmonary hypertension
Cardiac tamponade
Myocardial depression from metabolic problems
o Decreased filling of the ventricle will result in decreased stroke volume.
o Despite treatment, mortality rates for patients with cardiogenic shock range from
50% to 85%.
o Early manifestations
Tachycardia
Hypotension
Narrowed pulse pressure
myocardial O2 consumption
o Physical Examination
Tachypnea, pulmonary congestion (crackles, wheezes, course breathe
sounds)
Will give Lasix (push over 2 minutes), Albuterol with
Atrovent for pulmonary congestion
Want to monitor output and blood pressure after giving
Lasix
Pallor; cool, clammy skin
Decreased capillary refill time cyanosis in fingertips (if fingertips are
cool, pulse ox will not be right should be within 10 of the heart rate)
Anxiety, confusion, agitation
in pulmonary artery wedge pressure
Will have arterial line for pressures and frequent blood gases
Decreased renal perfusion and UO
o The early clinical presentation of a patient with cardiogenic shock is similar to
that of a patient with acute decompensated heart failure
o The hearts inability to pump blood forward will result in a low CO (<4 L/min)
and cardiac index (<2.5 L/min/m2)
o Tables 67-3 and 67-4 further describe the clinical presentation of a patient with
cardiogenic shock.
o Increase in PAWP heart not pumping ventricle filling LVEDP.
o Studies that are helpful in diagnosing cardiogenic shock include laboratory
studies (e.g., cardiac enzymes, troponin levels, b-type natriuretic peptide [BNP]),
electrocardiogram (ECG), chest x-ray, and echocardiogram.
o Will give Dobutamine

Hypovolemic Shock could be loss of blood or dehydration

o LOW BLOOD VOLUME
o Absolute hypovolemia loss of intravascular fluid volume
Hemorrhage, GI loss (e.g., vomiting, diarrhea), Fistula drainage,
Diabetes insipidus, Hyperglycemia, Diuresis
o Relative hypovolemia
Results when fluid volume moves out of the vascular space into
extravascular space (e.g., interstitial or intracavitary space)
Termed third spacing
One example of relative volume loss is leakage of fluid from the vascular
space to the interstitial space from increased capillary permeability, as
seen in sepsis and burns.
o Response to acute volume loss depends on
Extent of injury or insult, Age, General state of health
o Clinical Manifestations
Anxiety
Tachypnea
Increase heart rate
Decrease in stroke volume
PAWP
urinary output
If loss is >30%, blood volume is replaced
o Overall assessment of physiologic reserves may indicate the patients ability to
compensate. A patient may compensate for a loss of up to 15% of the total blood
volume (approximately 750 mL). Further loss of volume (15% to 30%) will

o
o

result in a sympathetic nervous system (SNS)-mediated response. This response

results in an increase in heart rate, CO, and respiratory rate and depth. Stroke
volume, central venous pressure (CVP), and PAWP are decreased because of the
decreased circulating blood volume.
Loss of autoregulation in the microcirculation and irreversible tissue destruction
occur with loss of more than 40% of total blood volume.
Common laboratory studies and assessments that are done include serial
measurements of hemoglobin and hematocrit levels, electrolytes, lactate, blood
gases, and central venous oxygenation (ScvO2), and hourly urine outputs

Neurogenic Shock
o DISTRIBUTIVE SHOCK
o Hemodynamic phenomenon that can occur within 30 minutes of a spinal cord
injury at the fifth thoracic (T5) vertebra or above and can last up to 6 weeks.
o Can occur in response to spinal anesthesia
o Results in massive vasodilation, leading to pooling of blood in vessels
o The injury results in massive vasodilation without compensation due to the loss
of SNS vasoconstrictor tone.
o Depression of the vasomotor center of the medulla from drugs (e.g., opioids,
benzodiazepines) also can lead to decreased vasoconstrictor tone of the
peripheral blood vessels, resulting in neurogenic shock.
o
o Initially, the patients skin will be warm owing to the massive dilation.
o As the heat disperses, the patient is at risk for hypothermia.
o Later, the patients skin may be cool or warm, depending on the ambient
temperature.
o Bradycardia instead of tachycardia..loss of SNS, and PS response
o Clinical Manifestations
Hypotension
Bradycardia is huge in neurogenic shock
Temperature dysregulation (resulting in heat loss)
Dry skin
Poikilothermia (taking on the temperature of the environment
o

Anaphylactic Shock
o Acute, life-threatening hypersensitivity reaction
Massive vasodilation
Release of mediators
capillary permeability
o Clinical Manifestations sudden onset of symptoms
Anxiety
Confusion
Dizziness
Sense of impending doom
Chest pain
Incontinence
Swelling of the lips and tongue, angioedema
Wheezing, stridor
Flushing, pruritus, urticaria
Respiratory distress and circulatory failure
o As capillary permeability increases, fluid leaks from the vascular space into the
interstitial space
o Anaphylactic shock can lead to respiratory distress
Caused by laryngeal edema or severe bronchospasm, and circulatory
failure, due to massive vasodilation
Septic Shock
o Septic shock has three major pathophysiologic effects

o
o
o

o
o

Vasodilation
Maldistribution of blood flow
Myocardial depression
Clinical Manifestations
coagulation and inflammation
fibrinolysis
Formation of microthrombi
Obstruction of microvasculature
Hyperdynamic state
Increased CO and decreased SVR
Tachypnea/hyperventilation
Temperature dysregulation
urine output
Altered neurologic status
GI dysfunction
Respiratory failure is common

Sepsis
Systemic inflammatory response to documented or suspected infection
Severe sepsis
Sepsis + Organ dysfunction
Septic shock =
Presence of sepsis with hypotension despite fluid resuscitation
Presence of tissue perfusion abnormalities
The main organisms that cause sepsis are gram-negative and gram-positive
bacteria. Parasites, fungi, and viruses can also cause the development of sepsis
and septic shock.
In as many as 10% to 30% of patients with sepsis, the causative organism is not
identified
MUST DO BLOOD CULTURE RIGHT AWAY TO ISOLATE
ORGANISM

Obstructive Shock
o Develops when physical obstruction to blood flow occurs with decreased CO
From restriction to diastolic filling of the right ventricle due to
compression
Abdominal compartment syndrome
o Patient will experience:
Decreased CO
Increased afterload
Variable left ventricular filling pressures
o Rapid assessment and immediate treatment are important.
o Pulmonary embolism and left ventricular thrombi cause an outflow obstruction as
blood leaves the right ventricle through the pulmonary artery.
o Other clinical signs include jugular vein distention and pulsus paradoxus.

Clinical Presentation of Major Types of Shock

Emergency Management

Stages of Shock
Usually not clinically apparent
Metabolism changes from aerobic to anaerobic.
Lactic acid build-up. ( LA is a waste product that requires oxygen for removal from the
body by the liver)
Not enough oxygen due to decreased tissue perfusion
Compensatory stage: reversible stage during which compensatory mechanisms are effective and
homeostasis is maintained.

STAGES OF SHOCK: PROGRESSIVE STAGE OF SHOCK

STAGES OF SHOCK: IRREVERSIBLE STAGE

Irreversible or refractory stage: compensatory mechanisms are not functioning

or are totally ineffective, leading to multiple organ dysfunction syndrome.

Diagnostic Studies

Specific Strategies for the Treatment of Shock

Fluid Therapy in Shock

Nursing Assessment
ABCs: airway, breathing, and circulation
Focused assessment of tissue perfusion
Vital signs, Peripheral pulses, Level of consciousness, Capillary refill
Skin (e.g., temperature, color, moisture), Urine output
Brief history
Events leading to shock, Onset and duration of symptoms
Details of care received before hospitalization

Allergies
Vaccinations

Nursing Process
Nursing Diagnosis or Priorities
Planning
Implementation
Evaluation

Shock to SIRS to MODS

If in Multisystem failure feet turn cyanotic (necrotic) and it starts to go up (will damage
GI, liver, kidneys)
Body is trying to save heart and brain

Diagnostic Studies for Shock

Thorough history and physical examination
No single study to determine shock
Blood studies
o Elevation of lactate
o Base deficit
12-lead ECG
Chest x-ray
Hemodynamic monitoring
Collaborative Care
Successful management includes
o Identification of patients at risk for shock
o Integration of the patients history, physical examination, and clinical findings to
establish a diagnosis
o Interventions to control or eliminate the cause of decreased perfusion
o Protection of target and distal organs from dysfunction
o Provision of multisystem supportive care
General management strategies
o Ensure patent airway.
o Maximize oxygen delivery.
Cornerstone of therapy for septic, hypovolemic, and anaphylactic shock = Volume
expansion

Isotonic crystalloids (e.g., normal saline) for initial resuscitation of shock

Colloids are effective volume expanders because the size of their
molecules keeps them in the vascular space for a longer period of time.
Despite this fact, colloids are costly, and no definitive studies
demonstrate that using colloids for resuscitation improves patient
outcomes.
o Volume expansion
If the patient does not respond to 2 to 3 L of crystalloids, blood
administration and central venous monitoring may be instituted.
Complications of fluid resuscitation
Hypothermia
Coagulopathy
Primary goal of drug therapy = Correction of decreased tissue perfusion
o Vasopressor drugs (e.g., norepinephrine)
If the patient has persistent hypotension after fluid resuscitation and
normalized CVP (8 to 12 mm Hg), a vasopressor (e.g., norepinephrine
[Levophed], dopamine [Intropin]) and/or an inotrope (e.g., dobutamine
[Dobutrex]) may be added.
o Achieve/maintain MAP >60 to 65 mm Hg.
o Reserved for patients unresponsive to fluid resuscitation
o Medications used to improve perfusion in shock are administered intravenously
via an infusion pump and a central venous line
Fluid replacement is calculated using a 3:1 rule (3 mL of isotonic crystalloid for every 1
mL of estimated blood loss).
o

SIRS

Systemic inflammatory response syndrome (SIRS) is a systemic inflammatory

response to a variety of insults.
Generalized inflammation in organs remote from the initial insult
Triggers
o Mechanical tissue trauma: burns, crush injuries, surgical procedures
o Abscess formation: intraabdominal, extremities
o Ischemic or necrotic tissue: pancreatitis, vascular disease, myocardial
infarction
o Microbial invasion: bacteria, viruses, fungi
o Endotoxin release: gram-negative bacteria
o Global perfusion deficits: postcardiac resuscitation, shock states
o Regional perfusion deficits: distal perfusion deficits

SIRS is manifested by two or more of the following conditions:

Temperature >38 degrees Celsius or <36 degrees Celsius.

Heart rate>90 beats per minute.

Respiratory rate>20 breaths per minute or PaCO2<32mmHg.
White blood cell count > 12,000/cu mm, <4,000/ cu mm, or >10% band forms.

MODS
Multiple organ dysfunction syndrome (MODS) is the failure of two or more organ
systems.
o Homeostasis cannot be maintained without intervention.
o Results from SIRS
SIRS and MODS Pathophysiology
Consequences of inflammatory response
o Release of mediators
o Direct damage to the endothelium
o Hypermetabolism
o Vasodilation leading to decreased SVR
o Increase in vascular permeability
o Activation of coagulation cascade

Last two systems to go down is

brain and heart

Signs of deteriation start from legs

(modeling, color of skin, decrease
pulseabdomen (kidneys, colon will
see sore in colon, decrease UO and
increase creatinine heart and lungs
(with ventilator the lungs still
pumping

Organ and metabolic dysfunction

o Hypotension
o Decreased perfusion
o Formation of microemboli
o Redistribution or shunting of blood
o Respiratory system
o Alveolar edema
o Decrease in surfactant
o Increase in shunt
o V/Q mismatch
o End result: ARDS
o Cardiovascular system
o Myocardial depression and massive vasodilation
o Neurologic system
o Mental status changes due to hypoxemia, inflammatory mediators, or
impaired perfusion
o Often early sign of MODS***
Renal system
o Acute renal failure if they survive they will need dialysis
Hypoperfusion
Release of mediators
Activation of renin-angiotensin- aldosterone system
Nephrotoxic drugs, especially antibiotics
GI system

o
o
o

Motility decreased: abdominal distention and paralytic ileus

Decreased perfusion: risk for ulceration and GI bleeding
Potential for bacterial translocation

o
o
o

Hypermetabolic state
o Hyperglycemia-hypoglycemia
o Insulin resistance
o Catabolic state
o Liver dysfunction
o Lactic acidosis
Will increase
Hematologic system
o DIC
Electrolyte imbalances
Metabolic acidosis

SIRS and MODS Collaborative Care

Prognosis for MODS is poor.
Goal: prevent the progression of SIRS to MODS
Vigilant assessment and ongoing monitoring to detect early signs of deterioration or
organ dysfunction are critical.
Prevention and treatment of infection
Aggressive infection control strategies to decrease risk for nosocomial infection
Once an infection is suspected, institute interventions to control the source.

Maintenance of tissue oxygenation

Decreased O2 demand
Sedation
Mechanical ventilation
Paralysis
Analgesia

Nutritional and metabolic needs

Goal of nutritional support: preserve organ function
o TPN, PPN
Total energy expenditure is often increased 1.5 to 2.0 times.
Use of the enteral route is preferred to parenteral nutrition.
Monitor plasma transferrin and prealbumin levels to assess hepatic protein synthesis

Support of failing organs

ARDS: aggressive O2 therapy and mechanical ventilation
DIC: appropriate blood products
Renal failure: continuous renal replacement therapy or dialysis

They still feel pain, indication,

increase BP, HR and
grimaces, need to give them
med

Know for test!!

o 10-15 question on shock and critical care
SIRs effect berating first
o CP reading, art line reading
MODs effect from
o 2 med questions
ground up
o 10-HIV
o HIV screening and testing on HIV
o Know ventilators for test - know setting up and helping with ventilation
o If high? If low?, Complication?