N418 – Exam 1
(1) OVERVIEW OF CRITICAL CARE – Unit 1
Critical Care Nursing
 The American Association of Critical Care Nurses (AACN) defines critical care nursing as the
specialty dealing with human responses to life-threatening problems (or potentially life-threatening
problems)
 Guides and puts out standards of practice that must be upheld if working in a critical care unit
 Problems can be actual or potential
 What are some examples of actual life-threatening problems?
o Gun-shot wound, acute MI, overdose, MVA
 What are some examples of potentially life-threatening problems?
o Attempted suicide, DVT, hypoglycemia, major surgical procedures (colorectal)
Essentials of AACN/CCRN- Critical Care RN
 Safe, competent care of critically ill with regards to medical dx (could be in ER, surgery, ICU);
meaning that the diagnosis guides the administration to a critical care unit
o Assessment – higher skill assessment level, advanced technology, assessment of EKG,
rate/rhythm, heart murmurs, etc.
o Diagnosis – assisting w/medical dx & nursing dx (ex: pt. on a ventilator has Dx of ineffective
airway clearance, ineffective gas exchange – work w/respiratory therapist, interpret ABG’s);
nurse gives the doctor the information they need to diagnose the patient
o Outcome Identification
o Planning – plan for post-op day 1 – what does pt. need to do, are they meeting outcomes; if
not what do we need to change/modify; assessment and interventions
o Implementation
o Interventions : things that are done to prevent the patient from having adverse event
o Education & Emotional Support (biggest education initiative currently is smoking cessation)
o Evaluation – are we meeting our goals, if not we need to re-plan, ongoing
o Collaboration/potential complications/risk for(s)
 Interpretation & Management of Cardiac Rhythms (will learn how to interpret & how to respond; rule
of thumb – anytime pt. has any type of cardiac monitoring you always treat the pt. and not the
monitoring)
o What are the only two rhythms we immediately defibrillate?  V-Fib & Pulseless V-Tach
o Remember – with lab walues/EKG/assessment findings, always look at trends
 Hemodynamic Monitoring (will learn the norms & gauge your interventions based on pt. levels to the
norms; will learn what to do, what’s typically done, what doctor may order)
o Non-invasive: BP, HR, Resp
o Invasive: Swan ganz catheter
 Circulatory Assistive Devices (LVADs)
 Airway & Ventilator Management
o Non-invasive: nasal canula, venti, etc.
o Invasive: ventilator, tracheostomy
o
o
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Pharmacology
o Some drips are allowed on regular floors (dopamine up to 5, insulin)
o Learn what’s used, not used, titrated, drips
o Most pharmacological agents are given IV route in the critical care setting
Pain (pain post-op or trauma is really acute pain but some could have chronic on top of acute pain
– learn how to recognize this)
o
o

If the patient is on room air and is in respiratory distress—put on 2L of oxygen.
FIO2 for the air we breathe is 21% (room air).
With patients in the critical care setting, the majority of the time they experience acute pain
(for less than 6 months)—this might require stronger narcotics or opioids.
If the patient is having anxiety and pain—always treat the anxiety first.
Sedation (conscious sedation used for procedures like cardioversions, EGD, colonoscopy; full
sedation uses Diprovan (Propofol) which causes full sedation & loss of respiratory function). Diprovan
normally used for pt on ventilator.
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N418 – Exam 1
Critical Care Specialty Units
 Developed as a result of the recognition that patients with acute, life-threatening illness/injury could
be managed more effectively if they were placed on specifically designated units.
Specialty Units
 General ICU
 CCU, SICU(surgical), MICU (medical emergencies like DKA)
 Special Populations (NICU, PICU)
 Specialties/Disease Process (neuro ICU, burn ICU)

Progressive/Intermediate Care Units (PCU pt. at risk for serious complications, but risk is lower than
ICU pt.)
o Use of PCUs provides critical care nursing for an at-risk pt. population in a more cost-effect
environment
o What are some monitoring capabilities of PCUs?
▪ Continuous EKG, arterial BP
▪ O2 saturation, end-tidal CO2
o What are some examples of pt. that can be found in the PCU?
▪ Scheduled for interventional cardiac procedures (stent placement)
▪ Awaiting heart transplant
▪
▪
▪
▪
Receiving stable doses of vasoactive IV drugs (Cardizem)
Being weaned from prolonged mechanical ventilation
---Pt. will move from specialty ICU when still critical but IS hemodynamically stable;
however, pt. still can’t be extubated so may move to an intubation unit
---Some pt. may move from ICU to LTAC – transition of where pt. go once out of
critical condition (based on condition, diagnosis, acuity level, and also insurance)
History
 Florence Nightingale described the advantages of placing pt. recovering from surgery in separate
areas (1800s).
 John Hopkins opened a 3 bed post-op neurosurgical ICU in the early 1900s.
 WWII & Korean wars influence the development of specialty units.
 Technological advances have had great influence on the development of specialty units.
 Critical Care Nursing:
o Critical Care Nursing as a “specialty” is less than 50 years old
o Critical Care Units opened across the country in the 60s
 The Critical Care Nurse:
o The critical care nurse requires an in-depth knowledge of A&P, pathophysiology (what
happens in the body with disease processes), pharmacology, and advanced assessment
skills.
o An astute nurse can prevent many complications and [significantly] contribute to good pt.
outcomes (will recognize a subtle change in hemodynamic monitoring, will notice subtle
changes and do appropriate interventions to prevent complications)
o Ex: Rhonchi can always be cleared with coughing; crackles is from fluid; can’t clear crackles
and rales with coughing so will give a type of diuretic to clear them or improve their cardiac
output with positive inotropes (digoxin, dobutamine, primacore)
o Adult Critical Care Nurses (ACLS) & Pediatric Critical Care Nurses (PALS)
 Nursing Roles:
o Certifications (1 or 2 years in an area of specialty ; study for an exam)
▪ CCRN (critical care nurse/certification)
▪ PCCN (progressive critical care nurse)
▪ CCN- Cardiac Care Nurse
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N418 – Exam 1
o
o
▪ Based more on nursing models
Advance Practice Registered Nurses (return to school for at least 2 years)
▪ CNS (mainly educates new nurses)
▪ NP, CNS, CRNA, CNM
▪ Based more on medical models
▪ Independently function from the doctor; prescriptive authority
ANCC- American Nursing Credentialing Center
▪ http://nursecredentialing.com/Accreditation.aspx
Critical Care Patient
 Patients are admitted to ICU because they are:
o 1) Physiologically Unstable (typically either BP/cardiac, resp., neurological, or GI that is
unstable)
▪ The things you do CPR for are the things that make you physiologically unstable
▪
▪
▪
o
Septic, hemodynamic instability
overdose
Ex: BP maintained by pressors, if too high and need continuous drip to lower it;
bradycardia, V-Tach, rigid/distended abdomen, paralytic ileus, etc.
2) At risk for serious complications (from sx, trauma, closed head injury – we need to monitor
them)
▪
▪
o
3) Require intensive, complicated nursing support and advanced technology (PA catheter,
LVAD, CRRT)
▪
▪
▪
▪
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These patients may not be unstable, but their chances for complications are greater.
“Example: patient went in for surgery and has more co-morbidities that puts them at
increased risk. They may bring them there to be able to monitor them and they may
progress well.”
“They may be on a vent, balloon pump, chest tubes or stumps, etc.”
PA Catheter
LVAD (left ventricular assistant device)
CRRT (continuous renal replacement therapy)
o 4) Require IV polypharmacy (sedation, thrombolytic, drugs that require titration)
Despite the emphasis placed on caring for individuals expected to survive, the incidence of death is
higher in ICU pt. than non-ICU patients. In general, non-survivors are typically:
o Older, have co-morbidities & experience longer ICU stays
Critical Care Environment
 Highly complex and highly technical (swan used to do hemodynamic monitoring)
 ICU is an uncomfortable place
 ICU Room Setup/Equipment:
o ECG Bedside/Invasive pressure cables (the nurse monitors their own EKGs in the ICU setting,
there are NO techs)
o BP cuff (individual use)/ NiBP (non-invasive blood pressure)
o Pulse oximetry (continuously)
o Suction gauges/canisters (3-4 maybe)
o Suction catheters
o Bag-valve mask (Ambu) – if a pt. is on a vent & has trouble breathing, the FIRST thing you do
is bag them; all pts in the ICU setting will have this at their bedside
o O2 flow meters, tubing, oxygen delivery
o IV poles, pumps with multiple chambers
o Bedside supplies (alcohol swabs, gloves, syringes, chux, etc.)
o Admission kit (basin, general hygiene supplies)
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N418 – Exam 1
o
The nurse is responsible to know that all of this equipment is functioning and working
Who Owns Comfort?
 The nurse!!!
 Comfort and pain are very different
o Rest (cluster care, give them adequate resting time)
o Positioning (prevents ischemia which causes pt. to feel pain)
o Loss of control, issues of trust, feelings of helplessness
o Isolation of social support (pediatric families will stay with them)
o
o
o
Pain is now considered one of the vital signs and comfort and pain take precedence over
anxiety
There is a move towards involving the family of an ICU patient more.
There is also a move allowing the family present during a code.
Common Problems of Critical Care Patients
 The pt. admitted to the ICU is at risk for numerous complications & special problems. Critically ill pt.
are usually immobile placing them at high risk for skin problems & venous thromboembolism. The use
of multiple, invasive devices predisposes the pt. to HC associated infections.
 Nutrition (enteral/parenteral nutrition; keep gut functioning if already working; enteral is best)
o Enteral feeding includes NG tubes, OG tubes, Dobhoff tubes (preserves the structure &
function of gut mucosa; stops the movement of bacteria across intestinal wall)
o Parental feeding includes PPN (peripheral line w/ mostly proteins) & TPN (central line with
essential elements, insulin, etc.)
o TPN – high risk for infection
o If the gut is functioning, keep it functioning and feed it.
o If you don’t feed the intestines, it will slow down and ileus occurs.
o “Abdominal compartmental syndrome- the swelling can push on the organs and cause some
o
o
o
o
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ischemia“
“Ecoli can translocate from the abdomen so if you keep the gut functioning and feed it, you
can keep the bacteria from growing and transferring”
Enteral, parental, TPN or PPN (difference is PPN is more protein, TPN is total and has
electrolytes, insulin, all sorts of things. TPN can only be given through central assess- PICC,
central line, etc. (not peripheral bc of the viscosity). You have to monitor CBGs with TPN.
PPN is given through peripheral access.”
The sooner they are fed, the better.
The metabolic demand of an ill patient is worse; therefore, they need nutrition (enteral or
parental).
Anxiety (treat pain before anxiety)
o What things can increase anxiety in ICU pt.?  Pain, impaired communication, sleeplessness,
immobilization & loss of control
Pain & Sedation
o “Most will be given IV, sometimes NG tube”
o
We need to determine if the pain is visceral or somatic.
o
Visceral pain radiates.
o
Does the patient have acute on chronic pain?
Impaired Communication (have to establish some non-verbal way to communicate w/ pt.)
o Yes- one blink
o No- two blinks
o If the pt has impaired barriers before they came in, it will be worse in the ICU
o Consult speech therapy
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N418 – Exam 1
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Sensory-Perceptual Problems (OA more at risk for sensory overload)
o Sleep deprivation can increase pain perception and anxiety
o Patients usually don’t get rest in the hospital; therefore sensory-perceptual problems
coincide with sleep
o Sensory overload
Sleep Problems (best thing to do to prevent is cluster care; except w/ increased ICP)
o Sleep-disordered breathing is a major concern in the ICU
o Decreased sleep duration & sleep loss influence pain perception
Noise in the ICU
 Telephone ringing
60-75 dB
 Raising/lowering side rails
90 dB
 O2, Chest tube bubbling/ventilator
70 dB
 Ventilator alarm
120 dB (loudest one; silence when suctioning)
 Cardiac monitor alarms
108 dB
 Call bells
50- 80 dB
 Ones that are built in for safety are the higher dBs
Patient Recollections of the Critical Care Experience
 Difficulty communicating
 Severe pain (like the fifth vital sign) or pain
that was not controlled
 Thirst (lemon-glycerin swabs, vasoline on
lips, pink toothetes)
 Difficulty swallowing
 Anxiety
 Depression
 Fear
 Lack of family/friends
 Physical restraints
o Not all intubated pt need to be
restrained
 Feelings of dread
o If a patient tells you they feel like
they are going to die or that
something is wrong – they are
probably right – don’t take this with
a grain of salt
 Inability to get comfortable
 Difficulty sleeping
 Loneliness
 Thoughts of death & dying
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N418 – Exam 1
Anxiety, Agitation, Delirium
 Anxiety is characterized by apprehension and autonomic arousal; an internal feeling (hyperaroused state – CNS)
o Anxiety is a hyper-aroused state (central nervous system arousal).
o
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
Can experience tachycardia and increased blood pressure.
Agitation is characterized by increased motor activity by patient (physical display)
o Pacing, fidgeting, etc
o Agitation is different from anxiety because it has to do with physical motor skills
Delirium is acute, reversible global impairment of cognitive processes—disorientation, impaired
short-term memory, altered sensory perception, and inappropriate behavior
o
o
o
o
o
o
“Do you know who the president is, what year it is, where you are, etc.”
“Usually look for the cause and try to reverse it”
Usually cause from electrolyte imbalances, DT tremors (alcohol withdrawal), etc.
If the patient is in the “light” delirium state, they may try to cover up their disorientation.
The patient might see things and hear voices (different than psychiatric disorders).
Sometimes the drugs that we give can also cause delirium.
Delirium & Dementia
 Delirium – fluctuations in mental status, inattention, disorganized thinking
o (Worsen clinical outcomes and increased LOS)
o Increases their length of stay and more medication is used to combat delirium – this worsens
outcomes
 Causes of Delirium:
o Lack of sleep – you want to make day day time and night night time and interrupt whenever
they have good condensed and uninterrupted sleep
o Oxygenation (brain is very sensitive to hypoxemia so if pt. very confused check O2 sat)
o Electrolyte imbalance (especially Na) the lower the sodium, the more abnormal behavior
that occurs – hyponatremia
o Drugs (narcotics, psychotropic)
o Hypoglycemia (act almost like a stroke pt.)
o Fever, Infection (especially in Geriatrics – OA with UTI is common example)
 Usually if an elder starts getting disoriented and confused – they usually have an
infection, either UTI or pneumonia
 UTI can cause dementia (usually the first sign) in an OA
 Sometimes these pt will not run fever – a small bladder infection can cause many
problems
 Dementia – slow, progressive, irreversible loss of intellectual or cognitive abilities like abstract
thinking, reasoning, pathological (higher risk for delirium when in critical care)
o More high level thinking is lost (e.g., principles of driving), but they will remember how to dress
themselves, etc
o You can always have delirium on top of dementia
 You can have an elder that has dementia and then come into the hospital and get some delirium
so its important to know the patients regular and baseline. The family usually is the best way to find
out what this is
Other Important Aspects
 Issues Related to Families/Caregivers (families’ major needs include information, reassurance &
convenience)
o Assess any issues family may have; explain all that can be done is being done
 Culturally Competent Care
o Death & Dying: some view advanced directives as a way to deny care, some view as a way
to prepare (open window to let spirits out; final bath for the deceased)
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N418 – Exam 1
What do you do after the death of a trauma pt.?  Don’t remove any lines or anything – this
is a coroner’s case; ALWAYS call LOPA & coroner (these two people are called for any
death)
Alternative/Complementary Therapies* - music, pastoral care, massage, pet therapy,
o

Organizations
 American Association of Critical Care Nurses (AACN)
o Offers Certification – CCRN
 Society of Critical Care Medicine (SCCM) – for physicians
Critical Care Campaigns
 We have guidelines for a lot of things that pt. may acquire in the hospital (UTI, hospital-acquired
pneumonia, etc.)
 Surviving Sepsis Campaign –
o 1.) Measure lactate level
o 2.) Obtain blood cultures prior to administration of antibiotics
o 3.) Administer broad spectrum antibiotics (always start on broad AB first; when C/S comes
back always check to see if pt. is on the right AB that the organism is most sensitive to)
o 4.) Administer 30ml/kg crystalloid for hypotension or lactate  4mmol/L
▪
Crystalloids include NS, LR, D5½; Colloids include things like albumin (volume
expanders)
TO BE COMPLETED WITHIN 6 HOURS…
o 5.) Apply vasopressors (for hypotension that does not respond to initial fluid resuscitation) to
maintain a meal arterial pressure (MAP)  65 mm Hg
o 6.) In the event of persistent arterial hypotension despite volume resuscitation (septic shock)
or initial lactate  4 mmol/L (36mg/dl):
o
▪ Measure central venous pressure (CVP)
▪ Measure central venous oxygen saturation (ScvO2)
▪ Bedside CV ultrasound
▪ Dynamic assessment of fluid responsiveness with passive leg raise
7.) Re-measure lactate if initial lactate was elevated
ICU Bundles
 Ventilator Bundles (prevent VAP: clean mouth, suction, TC&DB, weaning to lowest FI02)
o ABCDE Bundle –
▪ Awaken
▪ Breathe
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▪ Choose medications/coordinate care
▪ Delirium prevention
▪ Early ambulation
Central Line (protocol for changing dressings every so often, aseptic technique, accessing it,
swabbing it, antiseptic to clean it); change every 7 days
Multidisciplinary Rounds (goal is to identify anything that would prevent the pt. from progressing as
normal); where all the disciplines come and talk about what they can do to make things better
Goal Sheet (what you want the pt. to do on post-op days)
Glucose Control (CBG is >110 morning of bypass, pt. will be put on insulin drip – whether pt. diabetic
or not)
Sedation/Analgesia
Rapid Response Team
 A team of clinicians who bring critical care expertise to the bedside to help prevent them from
going to an ICU
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N418 – Exam 1
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*Based on 3 problems that can lead to failure to rescue (pt. does go bad and we don’t recognize it)
o Failures in planning (assessment, treatments – ex: failing to give a tx or giving a tx that
shouldn’t be given; gave BP medication w/out checking previous BP that was low)
o Failure to communicate
o Failure to recognize deteriorating patient condition
Why RRT?
o When reviewing the chart of patients that suffered cardiac or respiratory arrest you will find
▪ Subjective complaints (e.g., severe chest pain with EKG abnormalities)
▪ Vital sign changes (e.g., acute drop in blood pressure with syncope
▪
▪
o
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Telemetry changes
Nursing documentation preceded the event from hours to days in advance but no
action was taken
The pain thing with RRT is that we want to prevent from calling a code and prevent a
cardiac arrest
Key Features
o Must be able to respond immediately; must have critical care skills
Composition of RRT
o ICU nurse/ Medical Resident
o Hospitalist/Intensivist
o Nurse Supervisor
o Respiratory Therapy
An example of Outcomes
o 50% reduction in non-ICU arrests
o 58 % reduction of post-operative emergency ICU transfers
o Reduction in arrest prior to ICU transfer by 26%
Trigger Criteria for RRT: Respiratory
o ACUTE AND NEW
▪ Respiratory rate of <8 or >28
- PCA pump or opioid patients – stop the PCA and support the respiratory
component while calling the RRT
▪ 02 Sat < 90
- This could be normal for a COPD patient – no need to call RRT
▪ Threatened airway
Trigger Criteria: Cardiovascular
o ACUTE AND NEW
▪ Acute change in systolic BP to <90 (all depends on what that pts normal is though)
▪
▪
▪
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Acute sustained increase in diastolic BP> 110
Acute change in heart rate to <50 or >120
Onset of chest pain (cardiac chest pain cannot be reproduced by touching or
breathing in deep; if hurts to breath in deep or if you touch then it’s pleuritic pain)
▪ Acutely cold, pulseless, or cyanotic extremity
Trigger Criteria: Neurologic
o ACUTE AND NEW
▪ Confusion, agitation, delirium
▪ Unexplained difficulty to arouse
▪ Difficulty speaking or swallowing (could indicate stroke)
▪ Changes in pupillary responses

▪ Seizure
Trigger Criteria: Other
o ACUTE AND NEW
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N418 – Exam 1
▪
▪
▪
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Uncontrolled, out of proportion pain
Acute change in urine output (standard for post-op p.t is 30mL/hr)
Acute bleeding
▪ Acutely elevated temp
Rule of 100’s
o Heart rate  100
o Temperature  100
o SBP < 100
o Automatic consult to an ICU nurse and assessment and evaluation of pt. is done
Other Codes for Acute Issues
 These codes allow for everyone to be aware of what is going on (all team members)
 Code STEMI (ST elevation MI – pt. will go straight to cath lab)
o ST elevation myocardial infarction- needs to go right to cath lab”


o
Alerts the supervisor to call cath lab crew, EKG—everything ready to determine whether to
give the patient a fibrinolytic, etc.
o
Expedite the time so the patient’s outcome is improved.
Code Trauma
Code FAST
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N418 – Exam 1
(2) HEMODYNAMIC MONITORING – Unit 2
Definition & Purposes
 Hemodynamics is the study of forces involved in circulating blood – pump, pipes, fluid & electrical
conduction (this includes everything that controls homeostasis such as HR, BP, blood volume, etc.)
 Purposes of hemodynamics include to:
o Aid in the diagnosis of various disorders (includes what you can gather from non-invasive
monitoring such as BP, O2 sat, capillary refill, etc.)
- Hypertension (elevation in filling and ejecting)
o Assist in guiding therapies to minimize or correct dysfunction (use of Swan-Ganz to see how
therapy is working; use of ART lines to see how BP medication are affecting pt.)
- Patient is on a vasopressor drip or inotropic drip (increase the force of
conduction velocity of myocardial contractility)
o Evaluate the pt. response to therapy (watch for rise in CVP if giving pt. fluids)
Hemodynamic Monitoring
 Hemodynamic monitoring is the determination of the functional status of the cardiovascular system
– it is a measurement of pressure, flow & oxygenation within the system.
o It is used to assess (1) heart function, (2) fluid balance, (3) effects of fluids & drugs on CO
o
o

Using non-invasive tools, invasive catheters & highly technical monitoring systems the nurse can
evaluate a pt. (1) cardiac function, (2) circulating blood volume, (3) physiologic response to
treatment.
o

Cardiovascular system is a pump, with an engine (electrical conduction), pipes (deliver the
gas to the engine), and fluid (circulating volume).
Hemodynamic stability is affected by altering any of these parts.
Non-invasive:
 Blood pressure  can calculate the MAP
 Capillary refill
 Telemetry
 MAP (mean arterial pressure)—usually used to calculate end-organ tissue perfusion
(kidneys, gut, liver, etc)
 This tells us how well your organs are receiving oxygen and perfusion
 If MAP is low and the kidneys are not being infused, you will see a change in
urine concentration, BUN, creatinine, etc.
 When the kidneys aren’t perfused well—the renin-angiotensinogen system
kicks in—this affects blood volume and heart rate.
If the MAP is low in the kidneys, the kidneys are affected & you might see decreased BUN &
creatinine & urinary output (normal MAP is usually > 70mmHg)
Bedside Monitoring
 There are different levels of hemodynamic monitoring – patient in the ICU setting with non-invasive
or invasive monitoring
 The simplest level includes monitoring heart rate and rhythm and BP & end organ perfusion (MAP)
>>> central venous pressure (CVP) and intra-arterial blood pressure
o
o
o

Can’t evaluate whole heart function with one continuous rhythm strip.
If you see abnormalities with rhythm, you need other leads to determine if this is a problem.
Arterial line is a lot more accurate than a non-invasive blood pressure.
▪ With non-invasive you have to worry about cuff size, tightness, equipment function.
▪ If a patient has an automatic blood pressure machine that gives an abnormal
reading, the next thing we do is take a manual  then take it on the opposite arm.
For more sophisticated monitoring a pulmonary artery flow directed catheter (Swan-Ganz) might be
used.
o Indicated for anyone who is hemodynamically unstable (MI, septic shock, multi-organ failure,
requiring aggressive drug therapy that needs more invasive monitoring
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N418 – Exam 1
Indications for Hemodynamic Monitoring
 Used to monitor acutely ill individuals or those with cardiac disease undergoing surgery
o
o
o
o
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Depends on the patients co-morbidities
Heart attack, multi organ failure, septic shock, aggressive drug therapy that needs to be
invasively monitored (nitride, lepathed, neosynetrin)
Extensive surgery – large surgeries
Burn patients
Examples: multiple trauma victims, MI, shock (changes in BP, CO, CI), prophylactically for extensive
surgery, multiple organ dysfunction syndrome (MODS)
Cardiac Cycle
 Diastole – period of relaxation during which the ventricles are filling
o Period of relaxation during which the ventricle is filling
o Superior and inferior vena cava >> RA >> RV >> ??
o Depending on how much filling—there is a point of maximum recall.
o If you stretch beyond maximum recall, there will not be good contraction.
Diastole is the period of relaxation during which the ventricle is filling. nd ventricular muscle.
In a resting adult, each cardiac cycle lasts approximately 0.8 sec (800 msec). Atrial systole
requires about 0.1 sec, and ventricular systole about 0.3 sec. Atrial diastole lasts about 0.7 sec
and ventricular diastole about 0.5 sec during each cardiac cycle.
During the cardiac cycle, the pressure within each chamber of the heart rises in systole and falls
in diastole. The heart’s valves ensure that blood flows in the proper direction. Blood flows from
one heart chamber to another if the pressure in the chamber is more than that in the next.
These pressure relationships depend on the careful timing of contractions. The heart’s
conduction system provides the necessary timing of events between atrial and ventricular
systole.
During atrial diastole, blood from the superior and inferior vena cavae and the coronary sinus
enters the right atrium. The right atrium fills and distends, pushing the tricuspid valve open, and
the right ventricle fills. The same sequence occurs a split second earlier in the left heart. The left
atrium receives blood from the four pulmonary veins (two from the right lung and two from the
left lung). The leaflets of the mitral valve open as the left atrium fills and blood flows into the left
ventricle.
Ventricular systole occurs as atrial diastole begins. As the ventricles contract, blood is propelled
through the systemic and pulmonary circulation and toward the atria. The semilunar valves
close, the heart then begins a period of ventricular diastole during which the ventricles begin to
passively fill with blood and both the atria and ventricles are relaxed. The cardiac cycle begins
again with atrial systole and the completion of ventricular filling.

Systole – period during which chamber contracts & blood is ejected from the ventricle
o
o
Period during which the chamber is contracting and blood is being ejected from the ventricle
Electrolyte imbalance (K, Mg, Ca  in that order), anoxic (not enough O2 circulating),
hypoxic (in tissues) hypoxemia (in blood), and acidosis Interferes with contractility
The right atrium receives blood low in oxygen and high in carbon dioxide from the superior and
inferior vena cavae and the coronary sinus. Blood flows from the right atrium through the
tricuspid valve into the right ventricle.
When the right ventricle contracts, the tricuspid valve closes. The right ventricle expels the
blood through the pulmonic valve into the pulmonary trunk. The pulmonary trunk divides into a
right and left pulmonary artery, each of which carries blood to one lung (pulmonary circuit).
Blood flows through the pulmonary arteries to the lungs, where oxygen and carbon dioxide are
exchanged in the pulmonary capillaries, to the pulmonary veins. Carbon dioxide is exhaled as
the left atrium receives oxygenated blood from the lungs via the four pulmonary veins (two from
the right lung and two from the left lung). Blood flows from the left atrium through the mitral
(bicuspid) valve into the left ventricle. When the left ventricle contracts, the mitral valve closes.
11
N418 – Exam 1
Blood leaves the left ventricle through the aortic valve to the aorta and its branches and is
distributed throughout the body (systemic circuit).
Blood from the tissues of the head and neck is emptied into the superior vena cava. Blood from
the lower body is emptied into the inferior vena cava. The superior and inferior vena cavae carry
their contents into the right atrium.

The pressure on the left side of the heart is higher than the pressure on the right side of the heart
Cardiac Output
 CO is the volume of blood pumped by the heart in L/min from the ventricles
o Normal range of CO: 4 – 8 L/min
o Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate (HR)
o 5,600 mL = SV (70mL) x HR (80bpm)
o Reasons for decreased CO: volume loss, leaking protein
 Stroke Volume (SV) is the amount of blood ejected from the heart per beat – SV is affected by fluid
status (SV will decrease with dehydration; increase with fluid volume overload)
o Normal range of SV: 70mL
 If SV decreases, the HR will compensate by increasing so initially the CO remains the same.
 If HR increases, the SV will stay the same, but eventually it will decrease bc there is not enough time
for the ventricles to fill.
Cardiac Index
 Cardiac Index is the cardiac output adjusted for body size (more precise measurement of the
efficiency of the pumping action of the heart***)
Patient A
Patient B
Height
6 ft
5 ft
Weight
216 lb
118 lb
BSA
2.22 m2
1.50 m2
CO
4.0 L/min
4.0 L/min
CI
1.89 L/min/m2
2.4 L/min/m2
 The lower the body surface area (BSA), the higher the cardiac index *
 Typically, CI is ½ of CO so if the CO range is 4-8, the CI range is 2.4 – 4 (about half of cardiac
output)
 If a patient is larger in size, they have the same circulating volume, but they have more surface
area—therefore, the CI will be lower.

Cardiac output remains the same, but CI changes.

Rule of thumb – Cardiac Index is generally half of the cardiac output.

Remember—the right side of the heart is a low pressure system (only has to pump to the lungs);
the left side of the heart is a high pressure system (has to pump through systemic vascular
resistance).
Factors Affecting Heart Rate (HR)
 Autonomic Nervous System
o Sympathetic (SNS):
▪ Fight or flight which increases HR
o
▪ Caffeine, smoking, anxiety, fever, fear, adrenal tumor, renal failure, hypovolemia
Parasympathetic (PNS):
▪ Rest & digest which decreases HR
12
N418 – Exam 1


▪ Valsalva maneuver, vagal nerve stimulation
Medications
o Digoxin, Primacore, Dobutrex affect the pump
o Ca Channel Blockers & Beta-Blockers affect primarily electrical conduction
o Pressors, ACE Inhibitors & ARBs affect the pipes
o ***Any medication that is used to control HR can cause dysrhythmias
o HR increased by medications such as:
▪ Albuterol, Adderall Cocaine
▪ Epinephrine, Dopamine, Atropine
o HR decreased by medications such as:
▪ Beta-blockers
▪ Digoxin
▪ Ca Channel Blockers
Conduction Defect
o Abnormal rhythms that can result in an increased/decreased HR include:
▪ PSVT, SVT, runs of V-Tach, AV Blocks, V-Fib, A-Fib
Factors Affecting Strove Volume (SV)
 Preload (venous return)
o Preload is the amount of blood in the ventricles at the end of diastole
o PAWP reflects left ventricular end-diastolic pressure; CVP reflects right ventricular preload
o As preload increases, forces generated in contraction also increase, thus SV & CO increase
o Decreased by – acute blood loss, dehydration, diuresis, vasodilation, etc.
o Increased by – elevating pt. legs, exercising, administration of fluids
o
o
o
o
o
o
o

Afterload (vascular resistance)
o Afterload is the pressure that the ventricle must generate to empty its contents (refers to the
forces opposing ventricular ejection – includes systemic arterial pressure + mass & density of
blood)
o Typically indicated by systemic vascular resistance (SVR)
o Increased afterload usually results in decreased CO (can bring down the pt. afterload using
vasodilator therapy)
o
o
o
o
o
o
o

Low pressure
Into right ventricle
If you have less circulating volume, you have a decrease in preload.
If your patient is hypotensive but the volume is still the same, preload would decrease.
Sometimes it is not about the volume of blood, but how the blood gets to the heart (e.g.,
vasoconstriction or vasodilation).
Hemorrhage (blood loss), dehydration brought on by vomiting/diarrhea, hypotension (it
wouldn’t come back), meds (anti-hypertension)
Smooth muscle BP returns blood back to you
Afterload is affected by systemic vascular resistance (SVR)
SVR is based on systemic hypertension or hypotension
Amount of force the heart has to work to pump the blood out of the heart
If patient is hypotensive, the afterload is lower.
If patient is hypertensive, the after load is higher.
Forces against what it has to pump
Hypertension (more resistance through smaller opening)
Contractility (ejection fraction)
o Contractility refers to the force/strength of contraction resulting in ejection of blood from the
ventricles
13
N418 – Exam 1
o
o
o
o
o
o
o
o
o
o
o
▪ Normal range for EF: 60-80%
▪ EF warranting medical management is typically 40% or less
Increased contractility occurs when preload remains unchanged but the heart contracts
more forcefully (can be achieved with drugs called positive inotropes – Epinephrine,
Dopamine, Dobutamine, etc.)
▪ Results in increased SV & myocardial O2 requirements
Decreased contractility can occur with the use of negative inotropes (alcohol, Ca Channel
Blockers, Beta-blockers) & some clinical conditions (acidosis)
***If preload, HR & afterload remain constant yet CO continues to change, contractility is
most likely the cause (for example, it is reduced in HR)
Force of the muscle of the heart having to push the blood
If patient has heart failure, the contractility is decreased.
Myocardial tissues do not regenerate (don’t conduct electrical activity or pump like they
should).
Ejection fraction – left ventricle
Size of muscle, MI infarction, dec O2 to muscle, ischemia
No one have 100% ejection fraction – we probably have 80
<40% = problem
necrotic tissue does not contract like healthy tissue and does not electrical conduction
Blood Pressure
 Blood Pressure (BP) = Cardiac Output (CO) x Systemic Vascular Resistance (SVR)
 SVR is the amount of opposition to blood flow by the arterioles
 If you have change in either CO or SVR you will have a change in BP
 Higher BP = higher peripheral vascular resistance
 Sustained HTN = heart muscle hypertrophies*
Mean Arterial Blood Pressure (MAP) – (non-invasive BP)
 *Measuring end-organ tissue perfusion (lungs, liver, kidneys, etc)
 Systolic BP + 2 (Diastolic BP) ***
3
 Normal range for MAP: 70-105 mmHg (generally just want it >70)
Principles of Invasive Pressure Monitoring
 Invasive lines are used in the ICU to measure systemic & pulmonary BPs – equipment includes the
catheter, pressure tubing, flush system & transducer
 Referencing: means positioning the transducer so that the zero reference point is at the level of the
atria of heart
o Zero reference point is typically the stopcock nearest the transducer (place level with atria
by positioning it even with the phlebostatic axis)
 Zeroing: confirms that when pressure within the system is zero, the monitor actually reads zero
o Done by opening the reference stopcock to room air & observe the monitor for a reading of
zero
o When do you zero out the transducer?
▪ During initial setup, immediately after insertion of arterial line, when the transducer or
pressure cable has been disconnected & when the accuracy of the measurements
are questioned
 Perform a dynamic response test: done every 8-12 hours & when the system is opened to air or
measurement accuracy questioned (involves activating the fast flush & checking that equipment
reproduces a distortion-free signal)
 Obtaining BP measurements: when using an invasive line the readings from a printed pressure
tracing are most accurate at the end of expiration (position the pt. supine for initial readings)
14
N418 – Exam 1
Invasive Arterial Line/BP Monitoring (ART Line)
 Use of ART lines involves placement of a catheter into the radial, brachial, or femoral artery (most
commonly placed in the radial artery)
 Arterial line can be used for many purposes, including:
o Continuous arterial BP monitoring
o Obtain ABG samples
 Consists of a 3-way stopcock for flushing the line or for getting ABG samples
 Pressure bag normally applies 300mmHg & is set to 10-12 drips/min
 Indications for continuous arterial BP monitoring
o Acute Hypertension/Hypotension (pt. that require a drip to control BP)
o Shock
o Coronary interventional procedures (CABG, MVR, AVR)
o Head injury
o Multiple trauma
o Vasoactive drugs
o Respiratory failure
o Frequent ABG sampling
 Nursing Responsibilities
o Before ART Line Insertion: Allen’s Test
▪
o
Apply pressure to both the radial & ulnar arteries then release ulnar pressure – should
be visible & brisk blood return (3-5 seconds)
▪ If blood return is not witnessed, the ART line will NOT be placed (indicates absence of
patency in ulnar artery); will NOT be placed if pt. has carotid stenosis to that side as
well
After ART Line Insertion:
▪
▪
▪
▪

Assess pt. circulation q4h – referred to as CMS checks (Circulation, Mvmt, Sensation)
Nurse will be checking color, temperature, sensation, movement, presence of pain,
assess distal pulse, bleeding at site, capillary refill (this is all done to prevent
neuromuscular impairment)
Will typically see pt. with ART line in place that has an arm board so that the pt. can’t
bend their wrist which will cause erroneously high pressures
***If pt. says “I can’t feel my hand”, you need to call the MD bc the ART line is not
perfusing the pt. hand
Assessment
o Check equipment for proper set up:
▪ IV fluid (0.9% NS) with pressure bag & tubing to catheter; connection to transducer &
to monitor; check that alarms are on at all times; ensure dressing is occlusive
o Avoid heparin use due to risk of heparin-induced thrombocytopenia (HIT):
▪ HIT is the development of thrombocytopenia r/t administration of heparin or related
anticoagulants such as Lovenox (be sure to check pt. platelet count before giving
Lovenox)
▪ Caused by abnormal antibodies that attack platelets
▪
▪
▪
Predisposes pt. to thrombosis r/t excessive use of platelets (risk of DVT, PE, MI)
Determined when pt. experiences 50% reduction in platelets from baseline after use
Signs & Symptoms: fever, chills, tachypnea, tachycardia, SOB (due to thrombus
formation)
15
N418 – Exam 1
o



Components of a good wave form:
▪ Rapid upstroke & clear dicrotic notch – clear
end diastole point
Phlebostatic Axis (reference point):
o Mid-axillary line, 4th ICS (right below the nipple line)
o Closest to the level of right atrium
o Axis should be level with transducer (adequate measure of ART line or CVP)
o Will use this axis for ART lines & Swan-Ganz
o Position the pt. supine, flat or <45 degrees
o Zero out the reference point (stopcock nearest the transducer) – zeroing out usually done
once a shift or more if readings or not consistent
o If the transducer is higher than the axis, it will result in a false law reading (and vice-versa)
Flattened/Dampened waveforms may indicate several problems such as:
o Hypotension (not enough volume circulating
o Vasospasm
o Clot occluding the catheter
o Poor catheter placement/position
Complications of Arterial Lines
o Infection: site care is not usually done, because hopefully the arterial line will not be in for
more than 24-48 hours not long term
o Impaired circulation
o Hemorrhage (#1 is bleeding)
o Thrombus formation
o Neurovascular impairment or damage (reason it is important to check ulnar circulation)
 The catheter can be right on the radial nerve and can irritate it, may get some
numbness
o When taking it out (we can do this) hold for 10 minutes and/or pressure dressing (remember it
is an artery)
Pulmonary Artery Catheter (Swan-Ganz)
 Invasive/intravenous multiple lumen catheter which can be inserted at bedside in critical care areas
– this is a venous stick – into the subclavian or the internal jugular
 Some Swan-Ganz catheters are heparin-impregnated or lined (monitor for HIT – drop in platelets)
 Pulmonary Artery Catheters (Swan-Ganz) can be used to:
o Measure the pressure within the right heart (RAP/CVP – looks at preload & volume status)
 “RAP and CVP are used interchangeably. Right atrial pressure and central venous
pressure are the pressure in the right side of the heart.”

CVP measures preload and looks at the amount of circulating volume.

PAWP is an indirect measurement of left ventricular end diastolic function.
16
N418 – Exam 1
o
o
o
o
o
Measure the pulmonary artery pressure (PAP) & indirectly measure the left heart pressure
using PAWP (indirect measure of LVED)
Determine cardiac output (CO) (indirectly)
Obtain mixed venous/arterial samples
Infuse fluids
Continuously monitor a pt. SVO2

“The distal lumen comes out in the pulmonary artery, the proximal lumen will come out in the right
atrium. The thermistor connector measures the pts core temperature which is usually a degree
higher than an oral temp.

Svo2 mixed venous oxygen saturation in the pulmonary artery normal 65-80. Good way to tell
how much oxygen the patient is using and if they are getting enough”


***The balloon is only inflated upon insertion & when a PAWP is required
Nurse’s Role
o Prepare the pt., explain the purpose of the catheter & gather necessary equipment
o Before Insertion: note pt. electrolyte, acid-base, oxygenation & coagulation status
o Flush ports, maintain patency, obtain & evaluate readings
Insertion Procedure
o MD inserts catheter into the subclavian vein (or internal jugular), inflates the balloon & then
the catheter floats into the RA tricuspid valve RV pulmonic valve pulmonary artery
o Verify the placement of catheter through x-ray
o Pt. will be positioned sort of inverted to allow blood flow to assist with gaining access
o Balloon is then deflated to prevent necrosis of pulmonary artery
o The flow of blood carries catheter through (that’s why on right side and not left)

o
In the pulmonary system, the pulmonary artery receives deoxygenated blood and the
pulmonary vein receives oxygenated blood.
17
N418 – Exam 1
Catheter Placement
 The Proximal Port:
o Proximal port terminates in the RA – it is used to
measure RAP/CVP & to administer injectate for
measuring cardiac output
o CVP is basically a measure of preload, which is usually
affected primarily by fluid volume status (can
determine if pt. is in fluid volume overload or deficit
using CVP)
 The Distal Port:
o Distal port terminates in the PA – this allows for
continuous monitoring of PAP & obtaining mixed
venous/arterial blood samples (this is where blood
gets oxygenated)
o Also used to measure PAWP (“wedge pressure”)
(requires balloon inflation – NEVER leave it inflated >15
seconds)
o PA wedge pressure is an indirect measure of left
ventricular end diastolic pressure (LVEDP) – end of stretching (stretched as much as it can go
before it ejects)
 Balloon Inflation Port:
o Allows for the inflation of the balloon
Pulmonary Artery Catheter Readings
 Guidelines for evaluating readings from a pulmonary artery catheter (Swan-Ganz) include:
o Look at pt. trends – NOT just one number or reading
o Question abnormal results, recalibrate, recheck, look for supporting data cues
o Know what is normal for this pt. – determine what is acceptable for this pt
o Put the data together before drawing conclusions
 Right Atrial Pressure - CVP
o Monitored by attaching a transducer to the proximal port of PA catheter – transducer then
converts the pressure in the catheter into a waveform & digital readout
o Can also be monitored with the use of a central venous catheter (this method is more
common)
o Normal range for CVP: 2-8mmHg or 4-10 cm H2O
▪ Elevated CVP indicates right ventricular HF or volume overload; decreased CVP
indicates hypovolemia
o What does CVP tell you?
▪
▪
▪

If right atrial pressure is preload (volume) – if less then dehydrated
If CVP is 20 = volume overload
Reflects pressure in the right side of the heart OR pressure in the superior vena cava
▪ Reflects ability of the right side of the heart to manage fluids (e.g., preload)
▪ Serves as a guide to fluid volume deficit or fluid volume overload
o If CVP readings are elevated & pt. is in true volume overload, you may see some JVD
o Changes occur much later with CVP than pulmonary artery pressure changes
o Changes are slower in the CVP
 You will have pulmonary pressure changes first, before venous pressures
 Left sided HF causes right sided HF – this is why you will see changes in the pulmonary
artery before CVP
 Infusion port is more distal – takes longer – much later change???
Pulmonary Artery Pressure – PAP
o Obtained from the distal port of the PA catheter – the PAP is read as a systolic & diastolic
pressure (always lower than arterial BP in extremities)
▪ Normal range for PA Systolic: 15-30mmHg
18
N418 – Exam 1
o
o
o
o

▪ Normal range for PA Diastolic: 7-14mmHg
PAP is considered to reflect both right (directly) & left (indirectly) heart pressures
▪ PA Diastolic & PAWP are sensitive indicators of cardiac function & fluid volume status
▪ Monitoring PA pressures permits precise manipulation of preload
High PAP is caused by fluid volume overload, HF, MI, left ventricular hypertrophy
Low PAP suggests hypovolemia (low CVP & low CO)
***NOTE: readings are done at the end of expiration
Pulmonary Artery Wedge Pressure – PAWP
o Indirect measure of left ventricular end-diastolic preload – this is the ability to actually fill
o
▪ Normal range for PAWP: 6-12mmHg
If the wedge/balloon is overinflated, pt. will present with sort of like a tomb stone on the
wave form

Summary
o Proximal port > right atrium > RAP, CVP
o Distal port > pulmonary artery > PAP and PAWP (with the balloon inflated)

Measuring Cardiac Output (CO)
o Obtained by injecting a 10mL bolus of cool fluid (saline) into the proximal injectate port
(within the right atrium) within 4 seconds
o Time & temperature levels are evaluated & reading is obtained (thermodilution cardiac
output – TCO). Manual procedure
o Continuous Cardiac Output (CCO) uses a catheter which emits a pulsed signal – a
computer then measures a wave form (this is what is used currently)
Complications of Pulmonary Catheters (Swan-Ganz)
o Infection
o Air emboli (always close the line to the pt. by clamping at stopcock anytime line is
disconnected)
o Pneumothorax
o Thromboembolism
o Fluid overload
o Hemorrhage




“With the swann, you can cause v tach, and cause some damage if you keep it wedged for too long
too”
Anytime the patient has a central line, they are at risk for pneumothorax.
Power port cap on central line to reduce air emboli risk– so once you assess it the flap does not
open until you apply pressure (positive pressure cap) and then it closes after no pressure
Parameter
Equation
Normal Range
19
N418 – Exam 1
Arterial Blood Pressure (BP)
Systolic (SBP)
Diastolic (DBP)
90 - 140 mmHg
60-90 mm Hg
Mean Arterial Pressure (MAP)
SBP + (2 x DBP)/3
70 - 105 mmHg
Right Atrial Pressure (RAP)
2 - 8 mmHg
Right Ventricular Pressure (RVP)
Systolic (RVSP)
Diastolic (RVDP)
15 - 25 mmHg
0 - 8 mmHg
Pulmonary Artery Pressure (PAP)
Systolic (PASP)
Diastolic (PADP)
15 - 30 mmHg
4-12 mmHg
Pulmonary Artery Wedge Pressure
(PAWP) (LVEDP) or End Preload
6 - 12 mmHg
Left Atrial Pressure (LAP)
6 - 12 mmHg
Cardiac Output (CO)
HR x SV/1000
4.0 - 8.0 l/min
Cardiac Index (CI)
CO/BSA
2.5 - 4.0 l/min/m2
Stroke Volume (SV)
CO/HR x 1000
60 - 100 ml/beat
Systemic Vascular Resistance (SVR)
80 x (MAP - RAP)/CO
800 - 1200 dynes · sec/cm5
Pulmonary Vascular Resistance (PVR)
80 x (MPAP - PAWP)/CO
<250 dynes · sec/cm5
20
N418 – Exam 1
(3) MECHANICAL VENTILATION – Unit 2
Definition
 Process by which oxygen is moved in & out of the lungs by a mechanical ventilator
 Not curative, only supportive
 21% O2 – RA
 So mechanical vent is more than RA
Key Terms
 Tidal Volume (Vt): volume of air exchanged during a normal breath; normal volume of air
exchanged; 10-12 ml/kg or 6-8 ml/kg in acute lung injury
 Vital Capacity (VC): volume of air
exhaled with maximal effort after
maximal inspiration
o Pt. takes a big deep breath in
& exhales while pushing all the
air out
o Also indicates the most that
your lung volume can hold at
one time
 Fraction of Inspired Oxygen (FIO2):
o Concentration of oxygen
delivered to the pt.
o Room air is 21%
o Nasal Cannula
▪ 1L = 24%
▪ 2L = 28%
▪ 3L = 32%


▪ 4L = 36%
▪ 5L = 40%
▪ 6L = 44%
o Venti Mask
o Partial NRB
o 100% NRB
o BiPAP, CPAP
o Invasive ventilation (ET tube)
Total lung capacity includes both vital capacity & residual
Functional residual capacity is the volume of air remaining in the lungs after maximal exhalation
o This is what is used to direct treatment with PIP & CPAP (treatment increases amount of
residual air allowing for a longer time for air exchange)
o
o
o
Functional residual capacity is an important concept b/c this is what we manipulate with PIP
(positive in-expiratory pressure) & CPAP (continuous positive airway pressure)
Typically, when I exhale (even forcefully), there is some remaining air in the lungs. This
prevents the complete collapse of the alveoli, allowing some exchange of air throughout the
respiratory cycle (so that the PO2 does not drop significantly throughout the respiratory
cycle).
When we apply PIP or CPAP, we increase that amount of residual air. This provides for a
longer period of time for air exchange. It also prevents the alveoli from complete collapse,
giving you a bigger surface area for air exchange (this is another important concept for us).
Indications for Mechanical Ventilation
 Apnea or Impending Inability to Breathe:
o Who would be apneic?  Stroke pt. cardiac arrest, high cervical spine injury
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N418 – Exam 1
Pt. might exhibits signs & symptoms such as: hypoxia,
restlessness, decreased LOC, confusion, immobility,
accessory muscles use, difficulty speaking
o Impending inability means pt. respirations are labored &
they appear cyanotic – inevitable
Respiratory Failure: (use ABGs to determine if pt. experiencing
respiratory failure)
o pH <7.25 & PaCO2 >50mmHg (increased pH &
decreased CO2, increased rate – pneumonia & COPD)
When PaO2 & PaCO2 become almost equal
Normal PaO2 is greater than PaCO2
Severe Hypoxia:
o Requires FiO2 >50% to maintain adequate oxygenation
o PaO2 <60mmHg on oxygen therapy
o COPD will have higher PCO2 and a lower PO2
o Hypoxemia: low O2 in the blood/tissues (determined with ABGs)
Respiratory Muscle Fatigue:
o Neuromuscular problems such as ALS, Guillan Barre
o Stridor, tripod position while sitting
o Retraction, use of assessory muscles, workloader breather
Respiratory Rate >35 or <8-10
o Neuro patient with maybe a head injury to their resp system
o




Normal Arterial Blood Gas Values (ABGs)
 pH:
---7.35-7.45
 PCO2: ---35-45
 HCO3: ---22-26
 PO2: ---80-100
Artificial Airways
 Endotracheal Intubation:
o Tube is placed into the trachea via the mouth or nose past the larynx (mouth to trachea)
o ET intubation is more common in the ICU setting than tracheostomy
o
o
▪ Intubation can occur quickly & safely at the bedside
Indications for ET intubation include:
▪ (1) Upper airway obstruction, (2) apnea, (3) high risk of aspiration, (4) ineffective
clearance of secretions, (5) respiratory distress
▪ Only indicated for pt. expected to require less than 2 weeks on the ventilator
Assisting with Intubation:
▪
▪
▪
▪
▪
▪
Ambu bag available & attached to O2, suctioning equipment ready at the bedside
& IV access
Prepare for rapid-sequence intubation (RSI)
 Administration of both a sedative & paralytic agent during emergency airway
management (done to decreases risk of aspiration & injury)
 Sedative-hypnotic-amnesic such as Versed is used to induce unconsciousness
 Rapid-onset opioid is given to blunt the pain of intubation (Fentanyl)
 Paralytic drug such as succinylcholine is given to produce skeletal muscle
paralysis
Position pt. appropriately to allow visualization of the vocal cords (sniffing position)
Pre-oxygenate pt. using ambu bag & 100% O2 for 3-5 minutes (hyperoxygenate)
Confirm proper placement using an end-tidal CO2 detector (look for color or number
change)
Auscultate lungs for bilateral breath sounds & the epigastrium for the absence of air
sounds
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N418 – Exam 1
▪
▪

Observe chest for symmetric chest wall movement
Obtain ABG lab values within 25mins after intubation is confirmed to determine pt.
baseline oxygenation & ventilation status (continuous pulse-ox & end-tidal CO2
monitoring gives info about arterial status)
o Oral intubation: passed through the mouth & vocal cords then into the trachea – this is the
procedure of choice in emergencies
▪ Large bore tube is used which reduces the work of breathing bc there is less airway
resistance
o Nasopharyngeal intubation: placed blindly through the nose – used with pt. in which head &
neck manipulation/movement would be risky
▪ Contraindicated in pt. with facial fractures, suspected fractures of the base of the
skulls & post-op cranial surgeries (these pt. are more susceptible to kinky of the tube)
Tracheostomy Intubation:
o Surgical procedure performed if pt. needs ventilation for more than 2 weeks
o Tube is placed through a stoma that is surgically created in the neck
Nursing Management: Artificial Airways
 Maintaining Correct Tube Placement
o Place a mark on the tube where tube is placed r/t pt. lips or teeth q2h
o Confirm that the exit mark of the tube remains constant
o Continuously monitor for symmetrical chest movement & bilateral breath sounds
o Improper position of ET tube is considered a medical emergency – bag pt. immediately with
FiO2 100%


Maintaining Proper Cuff Inflation
o High-volume, low-pressure cuff stabilizes & seals the ET tube within the trachea & prevents
escape of ventilating gas
o Overinflated cuff can result in tissue erosion & a tracheal-esophageal fistula over time
o Cuff pressure is maintained at 20 – 25mmHg (assess & document cuff pressure q8h)
Monitoring Oxygenation & Ventilation
o Assess clinical findings related to oxygenation: ABGs, SpO2 & SvO2/ScvO2
▪ Assess for signs of hypoxemia: mental status changes, anxiety, dusky skin &
dysrhythmias
▪ PA or CVP catheters provide an indirect measurement of the pt. oxygenation status
o Indicators of adequate ventilation include: respiratory assessment findings & ABGs
▪ Assess pt. respirations for rate, rhythm & accessory muscles (hyperventilated pt. will
breathe rapidly & deeply with some numbness or tingling; hypoventilated pt. will
breathe shallowly & slowly with dusky appearance)
▪

PaCO2 is the best indicator of alveolar hyperventilation/hypoventilation
 Decreased PaCO2, increased pH indicates alkalosis
 Increased PaCO2, decreased pH indicates acidosis
o Hyperventilation – breathing rapid and deeply with circumoral and peripheral numbeness
and tingling
 PaCO2 is the best indicator of hyperventilation
(e.g., decreased PaCO2 increased pH indicates
respiratory alkalosis)
o Hypoventilation – breathing slowly and shallowly and may
appear dusky
 PaCO2 is the best indicator of hypoventilation
(e.g., increased PaCO2, decreased pH indicates
respiratory acidosis)
Maintaining Tube Patency
o Assess the need for suctioning by checking patency –
indicators of suctioning include:
23
N418 – Exam 1
▪


Visible secretions, sudden respiratory distress, suspected aspiration, abnormal breath
sounds, increased RR or sustained coughing, any changes in PaO2 or SpO2
o Closed suctioning: oxygenation & ventilation are maintained – minimal exposure to
secretions
▪ When do you perform this? – High PEEP, bloody/infectious secretions, frequent
suctioning
▪ Complications of suctioning include things such as: hypoxemia, bronchospasm,
increased ICP, HTN, hypotension, dysrhythmias
o Tracheal mucosal damage is likely with pressures >120mmHg, overly vigorous catheter
insertion & characteristics of the suction catheter itself
▪ Blood streaks or tissue shreds in secretions may indicate mucosal damage
o Thick secretions can be limited by ensuring hydration & humidification
▪ Do NOT instill NS into the ET tube (decreases SvO2)
▪ Postural drainage, percussion & turning pt. q2h can help move secretions
Providing Oral Care & Maintaining Skin Integrity
o Lips, tongue & mouth should be moistened with saline/water swabs to prevent drying
o Oral care includes: brushing teeth BID, suctioning q2-4h as needed, reposition & retape ET
tube q24h
Fostering Comfort & Communication
o Use writing or blinking as a way to communicate (reduces anxiety r/t inability to
communicate)
o Physical discomfort often requires sedation (Morphine, Ativan, Propofol)
Complications of ET Intubation
 Pain/discomfort
 Anxiety
 Infection (VAP)
 Aspiration (elevate HOB, suction as needed bc oral intubation increases salivation)
 Displacement of tube (regularly monitor lip placement)
 Obstruction of tube (secretions, mucus plug – this will trigger high-pressure alarm)
 Tracheoesophageal Fistula (overinflated cuff)
 Self-Extubation (signs include pt. vocalization, diminished breath sounds, respiratory distress, or
distention)
o Nurse is to stay with the pt., call for help, support the airway (Ambu bag) & secure the
appropriate assistance to immediately re-intubate the pt.
***Critical Alert
 Pt. has ET tube & condition changes (tachycardia/pnea, decreased LOC, etc.) CHECK THE TUBE!!!
 If vent is malfunctioning, use ambu-bag & bag them at FiO2 100%
Types of Mechanical Ventilation (Volume or Pressure)
NEGATIVE PRESSURE VENTILATION 
 Delivered as non-invasive ventilation & does NOT require artificial airway
 Used for pt. with chronic respiratory failure who require assisted ventilation for short periods of time
(spinal cord injuries, Guillan Barre, ALS)
 Increases & decreases pressure around the chest – causes changes in intrathoracic pressure
Negative pressure pulls chest outward forcing air to flow inward until machine cycles off &
passive expiration takes place (decreased intrathoracic pressure causes air to rush in)
Examples: iron lung, chest vest, body wrap & body suits
o

POSITIVE PRESSURE VENTILATION 
 During inspiration the ventilator pushes air into the lungs under positive pressure (intrathoracic
pressure is raised during lung inflation rather than lowered – expiration still occurs passively)
24
N418 – Exam 1

a. Non-invasive Positive Pressure Ventilation (NIPPV):
o Requires face mask, nasal pillows, or can be applied via ventilator & artificial airway
o Used short-term in weaning, after extubation or in acute respiratory insufficiency that is
expected to resolve quickly – may also be used to prevent intubation
o Used long-term in management of sleep apnea
o BIPAP:
▪
▪
▪
o
Delivers two different levels of positive airway pressure – Inspiratory pressure (IPAP) &
Expiratory pressure (EPAP)
Similar to pressure support ventilation bc the pt. must be able to spontaneously
breath & cooperate with treatment
Indicated for acute respiratory failure in pt. with COPD, HF & sleep apnea (NOT for
shock, altered mental status, or increased airway secretions)
CPAP:
▪
Continuous positive pressure to maintain conscious airway (usually in obstructive
sleep apnea)
▪
▪

Similar to PEEP in that they both keep alveoli opened but it is applied continuously
Caution pt. with myocardial compromise bc this increase the workload of breathing
– pt. have to breathe against the continuous pressure
b. Invasive Positive Pressure Ventilation
o Primarily used in acute care settings – requires artificial airway such as ET tube or
tracheostomy tubes
o Breaths are delivered until pre-set volume or pressure is reached (passive exhale)
o Volume Ventilation:
▪
o
Ventilator is controlled by pre-set volume (500mL of air is pushed in – intrathoracic
pressure is raised during lung inflation rather than lowered)
▪ It will deliver the pre-set volume regardless of changes in lung compliance or
resistance
▪ Exhalation occurs when inflow stops
▪ Volume is consistent with each breath, but airway pressures will vary
Pressure Ventilation:
▪
Ventilator delivers air until preset inspiratory airway pressure is present
▪
Disadvantage of pressure ventilation is that the tidal volume varies according to pt.
pulmonary system
 Hypoventilation & respiratory acidosis may occur in pt. with increased
resistance to flow or decreased compliance (ARDS)
With pressure ventilator, nurse MUST watch closely to ensure adequate tidal volume
▪
Settings & Modes for Vents
 Settings: based on pt. status including things such as ABGs, body weight, LOC, muscle strength
o Rate
o Depth (how much tidal volume do we want them to pull in?)
o Alarms (ensure they are always on)
o FiO2 (goal is to achieve optimal oxygenation with lowest FiO2 possible)
 Modes of Ventilation: determined by ventilatory status, respiratory drive, WOB & ABGs
o The mode of ventilation refers to how the vent works with the pt. own respiratory drive
1. Controlled Mandatory Ventilation (CMV) - volume
2. Assist-control Mechanical Ventilation (AC) - volume
3. Synchronized Intermittent Mandatory Ventilation (SIMV) – volume
4. Pressure Support Ventilation (PS) – pressure
5. Positive End Expiratory Pressure (PEEP)
25
N418 – Exam 1
Ventilator Settings
 Tidal Volume (TV): usually 10-12cc/kg
o Volume that you breath in & out with normal respiratory effort (depth of breath)
 Respiratory Rate (RR): this is the rate the vent is actually set at
 FiO2: lowest % to achieve PaO2 of at least 60%
 PEEP: usually 5-10 (avoid greater settings to avoid barotrauma & decreased CO)
 Pressure Support (PS): usually 5-10 (support needed to get through the tubing)
Modes of Ventilation
1. Controlled Mandatory Ventilation (CMV)
 Delivers preset volume at regular interval regardless of pt. inspiratory effort (set rate & tidal volume)
 Used in pt. with no respiratory effort or unable to breathe spontaneously – includes pt. such as:
o High c-spine injuries
o End-stage degenerative neuro disease
o Chemical paralysis aka anesthesia
 Used less often than Assist/Control
 Typically causes the pt. to panic & fight if they have any spontaneous respiratory effort bc they’re
trying to breathe with the ventilator
2. Assist-Control Ventilation (AC)
 Delivers preset volume or pressure when spontaneous breath initiated by pt. (pt. & vent share WOB)
o Preset rate ensures adequate ventilation
o Pt. can breathe faster than the preset rate but cannot breather slower than the rate
o Breath can be triggered by the pt. or can be time-triggered
 Used if pt. has: neuromuscular weakness, pulmonary edema or acute respiratory failure (pt. who are
breathing but not taking in enough volume)
 May cause respiratory alkalosis in pt. with high RR or respiratory acidosis in pt. with low RR
 Disadvantage: if it is too difficult for pt. to initiate breath, the WOB is increased & the pt. may tired &
develop ventilatory asynchrony (“fighting the vent”)
3. Synchronized Intermittent Mandatory Ventilation (SIMV)
 Preset rate during which a preset volume or pressure is delivered (mandatory ventilations)
o Allows pt. to breathe at own rate & volume between respirations
o Prevents respiratory muscle weakness
 Most used mechanism in the ICU setting (typically used for weaning)
o Unless a pt. in the ICU is chemically paralyzed, they will be placed on SIMV
 ***If the pt. is not initiating enough spontaneous breaths & the vent is set too low, the pt. O2 status
may decline resulting in inadequate support & oxygenation of the pt.
4. Pressure-Support Ventilation (PS)
 Present amount of pressure is delivered for a set time (duration of spontaneous breath)
 Pt. must be able to initiate breaths – pt. determines inspiratory length, tidal volume & respiratory rate
 Augments pt. spontaneous respiration & decreases work of breathing (decreases workload of pt. to
pull oxygen in & actually initiate a breath)
 Volume & pressure levels are affected by the pt. lung compliance
 Can be used with other ventilator modes or as a stand alone in weaning
 What are some advantages of PS ventilation?
o Increased pt. comfort, decreased WOB, decreased O2 consumption, increased endurance
conditioning (pt. exercises own respiratory muscles)
 NOT used as the sole ventilator support during acute respiratory failure bc of risk for hypoventilation
5. Positive End Expiratory Pressure (PEEP)
26
N418 – Exam 1






Ventilator maneuver in which positive pressure is supplied during exhalation (pt. exhale remains
passive, but the pressure falls to a level greater than 0 – usually 3-20cm H2O)
o During PEEP, lung volume during expiration & between breaths is greater than normal
o Major purpose of PEEP: maintain or improve oxygenation while limiting risk of O2 toxicity
Facilitates oxygenation by increasing surface area for gas exchange & preventing airway collapse
o Increases functional residual capacity (FRC)
o Maximizes number of alveoli available for O2 exchange
o Allows adequate oxygenation with less FiO2
Indications for PEEP
o Classic indication is ARDS (lungs are non-compliant & airway pressures not sent to heart)
o Lungs with diffuse disease
o Severe hypoxemia unresponsive to FiO2 >50%
o Loss of compliance or stiffness
o Pulmonary edema
Contraindications for PEEP
o Highly compliant lungs (COPD)
o Unilateral or non-uniform disease (atelectasis)
o Hypovolemia
o Low cardiac output
Physiological PEEP – 5cm H20
o >5cm can result in decreased cardiac output
o Do NOT increase PEEP for pt. with COPD or atelectasis
Complication of PEEP:
o Decreased cardiac output (decreased venous return bc of increased intrathoracic pressure)
o Increased ICP (decrease venous return – elevate HOB)
o Alveolar barotrauma & pneumothorax
o May stimulate RAAS release & later decrease renal function (decreased renal flow)
Complications of Positive Pressure Ventilation
 Pulmonary System: barotrauma, volutrauma, alveolar hypoventilation/hyperventilation, VAP
 Sodium & Water Imbalance: progressive fluid retention 48-72 hours after PPV, esp. PEEP
 Neurologic System: PPV esp. with PEEP can impair cerebral blood flow; may also have increased ICP
with JVD
 Gastrointestinal System: use of peptic-ulcer prophylaxis is recommended (Zantac, enteral nutrition)
 Musculoskeletal System: early progressive ambulation is one of the most important things to prevent
immobility associated problems
 Psychosocial Needs: pt. have an overwhelming need to feel safe – inform them, help them gain
control, help to give them hope
 Machine Disconnection/Malfunction: most deaths from disconnections occur when the alarm was
turned off – ALWAYS leave the alarms on
Special Considerations for Nursing Care
 Sedation (pt. with some cognitive ability needs to be sedated)
 Neuromuscular Blocking Agents
o Used to provide more effective synchrony with the ventilator thus increasing oxygenation
o Note: this does NOT provide sedation or analgesia
Weaning
 Process of reducing ventilator support & resume spontaneous ventilation
 Readiness for Weaning:
o Rapid Shallow Breathing Index (RSBI) – RR & average tidal volume over one minute
▪ Indication of whether or not the pt. is ready for weaning
▪ Normal RSBI: 60-105/L
▪ Indices for Weaning: <105/L
27
N418 – Exam 1
Compliance, Respiratory rate, Oxygenation, Maximal Inspiratory Pressure (CROP)
▪ Indices for Weaning: >13
Process of Weaning:
o Use of pressure support (PS) or CPAP is common
o T-piece with O2 for one hour (take pt. off vent for 1-2 hours & watch oxygenation – do ABGs
at the end of the hours & assess their status)
o Once-daily trial of spontaneous breathing (take off during day; put back on at night)
o Monitor SpO2, HR, RR, BP
o Return the pt. to the ventilator if pt. is in acute distress
o

Ventilator Associated Pneumonia Prevention Bundles (VAP)
 HOB elevation >30 degrees reduces frequency & risk for nosocomial pneumonia
 Prevention of DVT through the administration of thromboprophylaxis
o Weight-based dosage typically associated with treatment regimens (Lovenox 1-2mg/kg)
o Frequency-based dosages associated with prophylactic regimens (Lovenox 30-40mg/day)
 Use of peptic-ulcer prophylaxis reduces the risk of upper GI bleeding
o PPIs or H2 Blockers usually administered (Nexium, Protonix, etc.)
 Daily interruption of sedative drug (sedation holidays) infusions decreases the duration of
mechanical ventilation & length of stay in the ICU
o Diprivan & Precedex are some sedatives used for ventilation
 NG tube placement prevents aspiration of gastric content when vomiting & keeps gut functioning
 Intensive insulin therapy to maintain CBG <110 (reduces mortality & morbidity in critical care pt.)
 Daily screening of respiratory function followed by trials of spontaneous breathing (reduce duration
of mechanical ventilation, decrease complications & cost of ICU care)
 Mouth care q2h with chlorohexadine solution
 Suction, oral care, turn pt., maintain O2 status
***Ventilator Overview:
-What could cause a high-pressure alarm to go off?
 Biting the tube, kinked tubing, secretions (mucus plugs), and bronchospasm or pneumothorax
-What could cause a low-pressure alarm to go off?
 Vent becomes detached, pt. self-extubates
***A/C:
-A key concept in the AC mode is that the tidal volume (VT) of each delivered breath is the same,
regardless of whether it was triggered by the patient or the ventilator.
-If the patient does not initiate a breath before a requisite period of time determined by the set respiratory
rate (RR), the ventilator will deliver the set VT.
-**However, if the patient initiates a breath, the ventilator in AC mode will deliver the set VT; these breaths
are patient-triggered rather than time-triggered.
***SIMV:
-Like AC, SIMV delivers a minimum number of fully assisted breaths per minute that are synchronized with
the patient's respiratory effort. These breaths are patient- or time-triggered, flow-limited, and volumecycled.
-However, any breaths taken between volume-cycled breaths are not assisted; the volumes of these
breaths are determined by the patient's strength, effort, and lung mechanics.
-A key concept is that ventilator-assisted breaths are different than spontaneous breaths. High respiratory
rate setting on SIMV allows little time for spontaneous breathing (a strategy very similar to AC), whereas low
respiratory rates allow more time for spontaneous breathing.
Ventilator Modes Overview (Chart on Moodle)
MODE
FUNCTION
CLINICAL USE
28
N418 – Exam 1
Control Ventilation (CV)
Delivers preset volume or pressure
regardless of pt. own inspiratory
efforts
Usually used for pt. who are
apneic
Assist-Control Ventilation (AC)
Delivers breath in response to pt.
effort & if pt. fails to do so within
preset amount of time
Usually used for spontaneously
breathing pt. with weakened
respiratory muscles
Synchronous Intermittent
Mandatory Ventilation (SIMV)
Ventilator breaths are
synchronized with pt. respiratory
effort
Usually used to wean pt. from
mechanical ventilation
Pressure Support Ventilation (PS)
Preset pressure that augments the Often used with SIMV during
pt. inspiratory effort & decreases
weaning
the WOB
Positive End Expiratory Pressure
(PEEP)
Positive pressure applied at the
end of expiration
Used with CV, AC & SIMV to
improve oxygenation by opening
collapsed alveoli
Constant Positive Airway Pressure
(CPAP)
Similar to PEEP but used only with
spontaneously breathing pt.
Maintains constant positive
pressure in airways so resistance is
decreased
Independent Lung Ventilation
(ILV)
Ventilates each lung separately;
requires two ventilators and
sedation/paralysis
Used for patients with unilateral
lung disease or different disease
process in each lung
High Frequency Ventilation (HFV)
Delivers small amounts of gas at a
rapid rate (60-100 breaths/min);
requires sedation/paralysis
Used for hemodynamic instability,
during short-term procedures, or if
patient is at risk for pneumothorax
Inverse Ratio Ventilation (IRV)
I:E ratio is reversed to allow longer
inspiration; requires sedation/
paralysis
Improves oxygenation in patients
who are still hypoxic even with
PEEP; keeps alveoli from
collapsing
29
N418 – Exam 1
(4) COMFORT & SEDATION – Unit 2
Pain Management & Sedation: A Win-Win Strategy
 Humane/compassionate care
 Pain & discomfort elicit physiologic responses that are maladaptive (increased HR, BP, RR; cortisol
release; anxiety; can they participate in their own care?  repositioning, TCDB, etc.)
 Limits pt. ability to cooperate w/ pulmonary hygiene, weaning, mobilization & other aspects of care
 Pain, agitation & delirium are associated with poor outcomes (discharge criteria: have to be eating,
have to be back at baseline in terms of functioning,
 If have to treat pain and anxiety which do you treat first? PAIN
Physiological Responses to Pain & Anxiety
 Tachycardia- nl response to pain
 Tachypnea
 Hypertension
 Increased cardiac output (only initially)
 Pallor and/or flushing
 Cool extremities
 Mydriasis (pupillary dilation)
 Diaphoresis






Increased glucose production
(gluconeogenesis)
Nausea
Urinary retention
Constipation
Sleep disturbances
Atelectasis in bases of lungs from
breathing shallow
Difficult Dilemma: Pain & Anxiety are Inter-related
 One exacerbates the other (physiological response are very similar)
 If pain increases so does anxiety -if anxiety increase so can pain
 Anxiety contributes to pain by activating pain pathways
o Anxiety alters perception of pain (usually increased)
- If patient is hypoxic, they might have a decrease in pain threshold
o Increases aversion to pain & decreases tolerance of pain
- They wont be able ot tolerate what they used to be able to
o May increase the reporting pain
- May always report 10, but not grimacing and no increased HR – pain
perception may be higher due to anxiety
o Always treat the pain first & hopefully the anxiety will subside
 Nurses must accurately assess the problem – treating anxiety when pain is the problem (vice versa)
can lead to the escalation of both issues.
o Narcotics – work centrally – changes perception of change
o NSAIDS – work peripherally at the site
 IMPORTANT: assess pain & continuously, BUT independently
o Ask the patient
o PQRST: precipitating/alleviating, quality (stabbing, dull, sharp), radiation (des it radiate -abd
pain can raidiate down leg), severity (rating 0-10 or faces), timing (tells you acute or chronic)
Society of Critical Care Medicine: Multidisciplinary Document on Pain & Sedation
 Use of standardized scales necessary
 Treat pain first, then anxiety
 Morphine is the gold standard for acute pain (causes vasodilation – may also cause sedation,
hypotension, etc.)
 Drugs are not always the answer (pre-op teaching will help; pain r/t chest tubes will be relieved with
ambulation & removal; music, pet therapy, repositioning)
 Assessing Pain:
o Precipitating/alleviating factors – Quality – Radiation – Severity – Timing
Pain

The International Association for the Study of Pain defines pain as: “an unpleasant sensory &
emotional experience associate with actual or potential tissue damage” (tissue damage may result
from more than things such as trauma or wounds; can occur with IV sticks, invasive lines, etc.)
30
N418 – Exam 1

Whatever the pt. says it is, existing whenever the experiencing person says it does
o If they say 10/10 it is 10/10 no matter if they have high HR, etc.
o Some have high tolerance for pain
o Typically older people handle pain better – tolerance is higher
o Always want to find out if it is acute or chronic pain – may have underlying chronic issue that has
been going on for years

Acute Pain:
o Onset is sudden & duration is short-term (<3 months)
o Can be intermittent for 3 months
o May be brief, acute pain or acute persistent pain; can be episodic
o Accompanied by a high level of autonomic arousal (increase HR, RR, BP, anxiety, confusion)
o Associated with tissue pathology, injury, or surgery
o Some people will complain more about leg incision than a chest incision

Sources of Pain & Discomfort:
o Physical illness (myalgia pain), trauma (wound), surgery
o Monitoring devices (tight BP cuff)
o ET tubes, tracheostomy tubes, mechanical ventilation
o Routine nursing care (suctioning, dressing changes, position changes, ambulation)
o Prolonged immobility
Procedures Rated as Moderately-Severely Painful in ICU Patients
 ABG/Arterial line insertion

 Central line insertion

 ET suctioning

 ET tube in place

 Indwelling urinary catheter

Mechanical ventilation
Moving from bed to chair
NG tube insertion
IV insertion
Turning in bed
Pain Assessment
 The pt. self-report is the most reliable indicator of the existence & intensity of adult pain.
 P (precipitating factors) Q (quality – stabbing, dull, sharp, etc.) R (radiate?) S (rate 1-10) T (time)
 Nurses often assume that the pt. who is extremely ill, weak or confused cannot self-report pain
 Pain Scales:
o Visual Analog Scale
o Faces Pain Scale (Wong Baker’s Scale)
o Descriptive Scale (i.e. elephant on my chest, stubbing a toe, burning hand on stove, etc.)
o Behavioral Observation Scale (i.e. HR >140, grimacing, rapid respirations, rocking, crying)
 Pain History:
o Prior acute pain experiences – Ever had this pain before? What treated it? (OA typically do
well with just Tylenol for pain relief due to higher pain threshold; opioids typically alter LOC)
o Chronic pain: look for chronic pain on top of acute pain
o Usual relief measures (heat, cold, rest, stretching, NSAIDs, walking, etc.)
Nursing Management: Acute Pain
 Selecting the appropriate analgesic
 Evaluating when to administer the analgesic (give pain meds 30-45mins before PT; ATC)
 Evaluating how much to administer: you can always give lower medication than what the doctor
ordered
 Obtaining a change in prescription when needed
 ***IV  IM  PO  Transdermal – these are the routes of administration from fastest onset to slowest
SCCM Recommendations
 Scheduled analgesia recommended (ATC –avoids breakthrough pain & gets consistent serum level)
 Continuous infusions when control is difficult with scheduled doses (consider PCA pumps)
31
N418 – Exam 1


Use of slow-release medications recommended for de-intensifying therapy & providing baseline
analgesia
Use multiple approaches
Two Approaches to Pain Management
 Preventive Approach:
o Analgesics are given before the pt. complains of pain – given ATC not PRN
o Teach pt. not to wait until pain becomes a 10 before asking for medication
o Don’t wait until the pain becomes a ten before asking for medication.
o Oral pain medication takes a while to be absorbed and go through the system.
o “Around the clock – without the patient asking. Sets up a constant serum level.”
o Acute after Sx when pain will be severe because of Sx intervention
o Used to get pain under control
o Cancer patients
o PO or IV scheduled dose

Titration Approach:
o Adjusting & individualizing therapy based on the effect the drug is having on the pt.
o You can always use your judgment & refrain from administering entirety of ordered dose if it
seems like it is too high of a dose (can always give less but not more)
o Titration depends on the level of pain (moderate or severe)
PCA Pumps
 PCA pumps have a time interval between each possible dose – max of ____ ml/hr
o If the pt. pushes the pump before the next time interval, it will not administer a dose
 Educate the pt. about how the pump works
 Can have a PCA pump with just a basal, just a bolus dose, or both
o Basal is set so the pt. will get a pre-determined dose every hour like 1mg/hr; the bolus dose is
set up so if the pain control is not good enough the pt. can get extra medication by pressing
the button & bolus will have max)
 Another type is the epidural PCA – these do NOT provide bolus, typically basal rate (usually have
some equivalent pain med like Brevocain that acts as a nerve block)
Benefits & Risks of Analgesics
 Benefits:
o Reduced stress response symptoms, improves pt. comfort (HR hopefully goes down)
o Increased participation in care
(ambulation, toileting, etc.)
o If pt is sedated or neuromuscular block –
you do not have to admin pain medicine
 Risks:
o Respiratory depression #1(esp. narcotics;
increased risk for aspiration)
▪ Remember—respiratory depression
cannot occur in an individual who is
awake.
▪ Can have this with any route, but
more pronounced with PCA or IV 
directly into bloodstream so it
bypasses the first pass through the
liver where it is broken down
o GI motility reduction (constipation,
impaction, ileus)
▪ “Increased risk for ileus and constipation because slows gut down”
▪ Usually are put on Colace or have a suppository available
32
N418 – Exam 1
o
o
o
Additive sedation
N/V (Zophran more commonly ordered)
Pruritus (typically given Nubain which is used for pain but also relieves itching)
Schedule Narcotics (based on level of addiction)
 I: drugs with no currently accepted medical use & high potential for abuse (heroine, cocaine, meth)
 II: high potential for abuse, severe psychological & physical dependence (Hydrocodone, Adderall,
Demerol, Morphine, Fentanyl)
 III: moderate-low potential for dependence (Tylenol + codeine, testosterone, anabolic steroids)
 IV: low potential for abuse & low risk of dependence (Xanax, Valium, Benzos, Ativan, Ambien)
 V: lower potential for abuse than IV & contains limited amounts of certain narcotics (Lyrica, muscle
relaxer)
Analgesics for Acutely Ill Patients
 Opioid Analgesics (usually first line used)
o Morphine (Duramorph, MS Contin, Roxanol)
o
▪ This is the gold standard for analgesia
▪ Causes direct vasodilation
Fentanyl (Sublimaze IV or Duragesic patch)
▪
o
▪ Typically given during recovery or short procedures
Hydromorphone (Dilaudid)
o
▪ Used for pt. who are hemodynamically unstable
▪ Given if the pt. is allergic to Morphine
▪ Smaller dosing compared to Morphine
Meperidine (Demerol)
▪
▪



Good to use for weaning the pt. & chronic pain
Lowers the seizure threshold; not used as much
Be sure to always ask pt. about history of seizures
NSAIDS
o Ibuprofen
o Ketorolac (Toradol)
o When one NSAID does not provide relief, another should be tried due to various responses to specific
NSAIDs.
o NSAIDS should be limited to those who are at highest risk of adverse effects—elderly or history of
peptic ulcer disease
Non-narcotic analgesic
Acute pain and need immediate response – choose IV route
Morphine (Duramorph, MS Contin, Roxanol)
 Usually the gold standard
 Longer interval of action than fentanyl (longer duration or action/pain relief)
 Easy to titrate
 Available in various routes (PO, IV, IM, patch)
o Duramorph is typically used in surgery; MS Contin is long-acting morphine; Roxanol is given
sublingually & is very potent, used for cancer or hospice pt.
 Has active metabolite that can accumulate with renal insufficiency (high Creatinine and/or dialysis
pt.) & lead to prolonged sedation
o Decrease dose or decrease frequency of administration
o Cirrhosis, elevated LFTs, renal failure etc.  give less of a dose and/or less frequently
33
N418 – Exam 1


Causes direct vasodilation (hypotension) – NOT good for pt. who is hemodynamically unstable
o This effect makes it a useful drug for pt. with pulmonary difficulty (dilates bronchioles) & for pt.
with coronary pain (given if nitro doesn’t relieve pain)
o “Can cause hypotension- if pt is on bp medicine- this may not be drug of choice”
o Used for patients with pulmonary difficult (dilates and helps breathing)
o Coronary pain – dilates the coronary arteries
o If patient has low blood pressure issues or has labile BP—you will not choose this medication.
o Not for patients who are hemodynamically unstable
Can dilate when given IV over 2 min
Fentanyl (Sublimaze, Duragesic - patch)
 Rapid onset in acute distress
 Rapid onset in acute respiratory distress
 Hemodynamic stability (causes NO direct vasodilation thus you CAN give to pt. who is unstable)
o Doesn’t effect BP
o Can use for hemodynamically unstable pt
 Short duration with intermitted doses
 600 x greater strength (potency) than Morphine r/t lipid soluble (usually give 1/100th Morphine dose)
o Done with cancer patients or those patients with chronic pain
o You put the patch on—lipids absorb the medication through the fats
o Kept in a more controlled environment
 No renal dosing (CAN give it to dialysis pt. or pt. with renal insufficiency)
 Fentanyl Patches (Duragesic)
o Provides low constant dose (change patch q72h, rotate sites)
o Questionable absorption with edema or diaphoresis (swelling & third-spacing might slow
absorption)
o Used in weaning pt. off of pain medications
o Often used with cancer pt. along with MS Contin
Hydromorphone (Dilaudid)
 No direct vasodilation – use this for pt with problems with BP
 Longer duration of analgesia compared to Fentanyl
 Lack of active metabolite – good for renal insufficiency or pt. with low BP (safe when pt. is
hemodynamically unstable)
 Stronger than morphine
Meperidine (Demerol)
 Avoid repeated dosing
o Active metabolite (Normeperidine): accumulates in renal insufficiency – neurotoxic
o CNS Stimulant:
▪ Tremors, agitation, psychosis, seizures (typically do not give to OA pt.)
 Sometimes used for GI distress bc Demerol relaxes the sphincter of Odi better than other
medications
 Contraindicated: pt. with acute pain lasting more than 2 days or requiring large doses
 Not preferred because when passes through liver it creates active metabolites which makes it stay longer
 “Sometimes used for GI issues – it relaxes sphincter of Oddi”
 Contraindicated for patients with acute pain lasting more than 2 days and for those in whom large doses
(more than 600mg per 24 hours) are needed.
 Should not be used to treat chronic pain.
 A hyperpyrexic syndrome with delirium, which can cause death, can occur if meperidine is given to patients
taking an MAOI.
NSAIDS (works at the site; opioids work centrally)
 Ketorolac (Toradol):
o Non-sedative/non-respiratory effect
▪
350 x stronger than aspirin
34
N418 – Exam 1
o
o
o
▪ PO, IV, IM, Gtt
▪ 30 mg = 10-12mg Morphine
Opioid sparing – using Toradol allows you to give 25-50% less morphine (synergistic effect)
Change dosages based on renal function (can cause increased creatinine; caution in OA)
▪ In presence of renal insufficiency, dose is usually decreased to 15mg
Given no longer than 5 days due to increased bleeding & increased renal indices
Agonist-Antagonist Agents
 (1) Nubain (relieve itching, sedates pt.), (2) Buprenex, (3) Stadol (anesthesia adjunct)
 Causes less respiratory depression, but more dysphoria & agitation
 Use extreme caution due to potential to precipitate withdrawal in chronic opioid users
Alternate Pain Control
 PCA: IV/epidural (also Dilaudid, Morphine)
 Epidural: usually used for thoracic/abdominal surgery
(colon resection, lobectomy)
o Fentanyl/Bupivacaine (increased respiratory
sedation, CMS, epidural hematoma)
o Epidural hematoma is an emergency – can
happen sometimes when pt. is on Lovenox &
have increased bleeding time & they puncture
the epidural space for procedure
 On Q Ball: squishy ball they fill with medication
attached to a tube inserted into the site of surgery –
when pt. is in pain they squeeze the ball which puts
medication internally into the area (used a lot for
thoracic or abdominal surgeries)
WHO Pain Ladder
1. Use a non-opioid (NSAID, Acetaminophen) or an adjuvant (Xanax) or both
2. If pain persists or increases, use an opioid for mild-moderate pain (Codeine, Tramdaol) & non-opioid
or adjuvant
3. Opioid for moderate-severe pain (Morphine, Dilaudid) & non-opioid and adjuvant
4. Cancer pt. – you want true pain relief bc their pain is not going to go away; typically see them on
pathes, Roxanol, Xanax, analytic, etc.
SCCM Clinical Practice Guidelines
 If IV analgesia is required, Fentanyl, Dilaudid & Morphine are the recommended agents
 Fentanyl is preferred for rapid onset of analgesia in acutely distressed pt.
 Fentanyl or Dilaudid is best for hemodynamic unstable pt. or pt. with renal insufficiency
 Morphine & Dilaudid are preferred for intermittent therapy bc of longer duration of action
Equianalgesia
 To provide equal analgesic effect with new agents
 Conversion Equivalence conversion (how do you change from PO to IV & get same pain relief?)
 Several apps: Opioids Conversion
What to use other than drugs?
 Family
 Music
 Massage, lighting
 Positioning
 Temperature
 Sleep


Spirituality
Pet Therapy
35
N418 – Exam 1
Inadequate Treatment of Pain
 There are four common misconceptions regarding opiate use that contribute to inadequate
treatment of pain – these include:
o Fear of addiction (opiophobia)
o Fear of physical dependence – if truly in pain there will be no physical dependence
o Fear of tolerance
o Fear of respiratory depression
Under-treatment of Pain
 Oligoanalgesia: practice of treating pain with minimal drug use (MD thinks pt. not really in pain)
 Like the elders woman that could probably be treated with Tylenol alone
 Do this because the practitioner thinks the pt is not truly in pain
 Pt may be drug seekers
Sedation
 Process of alleviating nervous excitement (benzo – drug of choice)
 Goal is to have a calm pt. that can easily be aroused with maintenance of a normal sleep schedule
 Sedation is measured using: sedation-agitation scale (SAS) & the motor activity assessment scale
Anxiety Management (SCCM)
 Rule out other causes for the anxious behaviors – some other causes include:
o Hypoxia, hypoglycemia, sensory overload, drug interactions, sleep deprivation, pain, fear
 Once other causes have been ruled out move to medications with a plan
 Most desirable to have PRN orders
 Unless on DT (deprevation/tremor) protocol not scheduled
 Benzodiazepines cause dependency; therefore you should not abruptly stop this medication if the
patient has been on this medication for a while
Sedation Measurement
Sedation-Agitation Scale (SAS)
 Helps to separate sedated pt. into those you can eventually wake up (3), those you can’t awaken
but can arouse (2) & those you can’t arouse (1)
7
Dangerously agitated
Pulls at ET and other tubes, climbs
6
Very agitated
Does not calm despite verbal reassurance,
requires physical restraint, bites ET
5
Agitated
Anxious or mildly agitated, attempts to sit
up, calms down in response to verbal
warnings
4
Calm & appropriate
Calm, awakens easily, follows commands
*Where you want them
3
Sedated
Is difficult to arouse, awakens to verbal
stimulation, follows only simple commands
2
Very sedated
Arouses to physical stimuli but does not
communicate or follow commands
1
Un-arousable
Has minimal or no response to noxious
stimuli (smell, sternal rub, push pen against
the nail-bed), does not communicate or
follow commands

36
N418 – Exam 1
Sedation Measurement
Motor Activity Assessment Scale
0
Unresponsive
Does not move w/ noxious stimuli
1
Responds only to
noxious stimuli
Opens eyes OR raises eyebrows OR turns
head toward stimuli OR moves limbs
2
Responds to touch or
name
Opens eyes OR raises eyebrows OR turns
head toward stimuli OR moves limbs
3
Calm and cooperative
No external stimuli is needed to elicit
response, and pt. is adjusting sheets/clothes
purposefully
4
Restless and
cooperative
No external stimulus is needed to elicit
response, and pt. is picking sheets/tubes,
uncovering self. Follows commands.
5
Agitated
No external stimulus is required to elicit
movement AND sitting up OR moves limbs
out of bed AND does not consistently follow
commands
6
Dangerously agitated
No external stimulus required, pulling tubes
OR thrashing OR trying to climb out of bed
and does not calm down when asked
Sedatives Used in Critically Ill Patients
 Benzodiazepines (most used)
o Midazolam (Versed – used for conscious sedation – pre-op, cath lab; causes amnesia)
o Diazepam (Valium – typically used for seizure pt. & status epilepticus)
o **Lorazepam (Ativan – used for long-term sedation – used for seizures, agitation, etc.)
o ANTIDOTE FOR BENZODIAZEPINES  Flumozenil (ROMAZICONE); do NOT give to pt. with history
of abuse
 Nonbenzo Sedative
o Propofol (Diprivan) – needs airway support so pt. HAS to be intubated
▪ Michael Jackson drug
▪ Substance that is very short acting
▪ Good to use for patients on a ventilator who you want to stop the Diprivan—it will take less
than a couple of minutes for them to become awake and alert.
▪ Pts must be intubated if used as a drip
▪ Can be used as a IVP for cardioversion
 Selective Alpha-2 Receptor Agonist
o Dexamedetomidine (Precedex)
 ** Recommended for long term sedation
Propofol (Diprivan)
 In low doses, Diprivan induces a state of deep sedation
-Most of these do not provide for amnesia (forget what has happened)
 Short half-life, pt. can be fully conscious within 30 minutes after stopping infusion
 Slows cerebral metabolism & decreases an IICP (sedative of choice w/ closed-head injury or bleed)
 Not very reliable in terms of amnesic effect – pt will remember
37
N418 – Exam 1

High lipid content (delivers 1.1 kcal/mL as fat) – all tubing & solution must be changed q12h (tubing
is harder & has a more yellowish color than normal tubing)
o Patient is at risk for infection (if it is going into a central line—it has lipid content)
o Special tubing is required (if you have regular tubing, the propofol will be absorbed into the tubing).
o Pts who are on it for long periods of time have a higher risk for sepsis d/t high lipid content



Pt. must be intubated if Diprivan is going to be used as a drip
Diprivan is used IVP in Cardioversion (spontaneous respiration still occurs if given IVP)
Contraindications: allergy to eggs, egg products & soy
Dexemedetomidine (Precedex)
 Short-term sedative for mechanically ventilated pt.
 Decreases NE levels (so nurse can see if pt. is tachycardia or sympathomimetic response)
 Reduces brain noradrenergic activity
 Inhibits sympathetic activity (decreases BP & HR) (alpha agonist)
 Reduces need for add-on morphine
 Minimal amnesic effect
 Use caution in unstable pt. due to more pronounced hypotension & decreased sympathetic
response (bradycardia)
 ***Still address them as a pt. who is awake/alert because they will remember what they hear
Levels of Sedation
 Light Sedation (minimal sedation; relief of some anxiety)
o Pt. can still follow commands
o Cognitive function & motor coordination may be impaired
o Ventilation & CV function unaffected (not hypertensive, adequately sedated – where you
want the pt. to be)
o ***Ex: Pt. who has an anxiolytic such as Xanax
 Moderate Sedation with Analgesia (conscious sedation, procedural sedation)
o Conscious sedation requires nurse to be certified
o Depression of consciousness during which pt. respond purposefully to verbal commands &
when shaken
o Pt. maintains his own airway
o CV function usually unaffected, however respiratory IS affected
o Typically used for someone having their wisdom teeth pulled, cardioversion, colonoscopy
 Deep Sedation & Analgesia
o Depression of consciousness during which pt. cannot be easily aroused but may respond
purposefully after repeated or painful stimulation
o These pt. requires assistance in maintaining a patent airway (bagging, ET tube, LMA)
o CV function is usually maintained
 General Anesthesia (highest level of sedation; total loss of consciousness)
o Usually give you a sedative before they put you under general anesthesia





Conscious sedation can only be done with recovery
o In a secure area where if they need to be ventilated they have the equipment (controlled
environment)
Anxiolytic
Moderate – This is what we will do conscious sedation on a patient
o Nurse who performs conscious sedation needs to be ACLS certified.
o Airway does not need any artificial airway
o No drop in blood pressure or heart rate
Deep Sedation – Where we start having some changes
General Anesthesia
o Unarousable, even with painful stimulation
38
N418 – Exam 1
ASA Definitions of General Anesthesia and Levels of Sedation/Analgesia
Minimal Sedation
(Anxiolytic)
Moderate
Sedation/Analgesia
(Conscious
Sedation)
Deep
Sedation/Analgesia
General
Anesthesia
Responsiveness
Normal Response
to Verbal
Stimulation
Purposeful response
to verbal or tactile
stimulation
Purposeful response
after repeated or
painful stimulation
Unarousable, even
w/painful stimulus
Airway
Unaffected
No intervention
required
Intervention may be
required
Intervention often
required
Spontaneous
Ventilation
Unaffected
Adequate
May be inadequate
Frequently
inadequate
Cardiovascular
Function
Unaffected
Usually maintained
Usually maintained
May be impaired
o
Over-Sedation
 State of unintended pt. unresponsiveness in which the pt. resides in a state of suspended animation
that resembles general anesthesia
 Go past the barrier of therapeutic sedation for the procedure
 Narcan is given for narcotics/opioids; Romazicon is given for benzos
 Run into trouble in those with renal impairment, COPD with O2 at home, etc. (use caution)
Too Little Sedation
 Risk of self harm
 Unplanned extubation/intubation in restless, anxious, agitated pt. occurs in 8-10% of intubated pt.
after an average of 3.5 days in the ICU (places pt. at risk for self-harm)
 Of these self-extubation cases, 6% cause significant complications (Aspiration, Dysrhythmia,
Bronchospasm, Bradycardia)
Delirium
 Acute onset, usually seen a lot with ICU pt. (CAM: Cognitive Assessment Measurement in ICU –
ongoing assessment to ID earlier those pt. moving to delirium stage)
 Delirium occurs in up to 87% of mechanically ventilated pt. in the ICU
o Associated with increased mortality/morbidity, longer ICU stay & more health care costs
o 98% of nurses routinely assess sedation level whereas only 47% assess for presence of delirium
 Assessing for Delirium (signs & symptoms)
o Reduced awareness of the environment:
39
N418 – Exam 1
▪
▪
o


Inability to stay focused on a topic, still smart in the beginning stage (don’t ask
specific date maybe ask what day of the week, month, year)
Wandering attention (esp. OA at night)
▪ Getting stuck on an idea rather than responding to questions or conversation
▪ Being easily distracted by unimportant things
▪ Being withdrawn, with little or no activity or little response to the environment
Poor thinking skills (cognitive impairment):
▪ Poor memory, particularly of recent events
▪ Disorientation, or not knowing where one is, who one is, or what time of day it is
▪ Difficulty speaking or recalling words
▪ Rambling or nonsense speech
▪ Difficulty reading/writing
o Behavior changes:
▪ Seeing things that don’t exist (Hallucinations)- lots of times see family members that
are not living
▪ Restlessness, agitation, irritability or combative behavior- might think that they are in
their house and you are breaking in trying to steal something; or that you’re trying to
restrain them
▪ Disturbed sleep habits
▪ Extreme emotions, such as fear, anxiety, anger or depression
Causes of Delirium:
o Neurological (TIA, meningitis,
encephalitis, brain abscess)
o MI
o Infection
o Respiratory hypoxia, PE
o Alcohol withdrawal
o Glucose
o Metabolic Issues (esp. Na)
Treatment of Delirium:
o Correct the cause first if this is
possible by identification of true
cause
o Neuroleptic Medications:
▪ Haloperidol (Haldol) is
usually the drug of choice;
sometimes Ativan is given
 Delivered via IM or
IV
 10-20min onset &
lasts
for hours
 SE: extra-pyramidal
symptoms (EPS)
increase with
benzo (NMS, Torsades) use
 AVOID giving this medication to pt. with Parkinson’s
o Antipsychotic:
▪ Olanzapine (Zyprexa)
Stir-Up Post Anesthesia
 TCDB
 Incentive Spirometer q2h about 10 breaths per hour
 Movement of legs
40
N418 – Exam 1



Ambulation
Turning in bed
***This is all done to prevent atelectasis
41
N418 – Exam 1
(5) CORONARY ARTERY DISEASE – Unit 3
ASCVD – Arteriosclerotic Cardiovascular Disease
 Type of blood vessel disorder that is included in general category of atherosclerosis (can be with
any artery – anything with an arterial lumen has the potential to develop atherosclerosis)
 Atherosclerosis is the major cause of CAD
o Most of the deaths related to CAD are due to MI, HF, pericarditis
 Focal deposit of cholesterol & lipids in the intimal wall of the artery
 Other causes of injury to the intimal lumen of artery include:
o Tobacco use, HTN, DM, some infectious processes
Development of Plaque
 Occurs over many years – progressive disease
 Usually starts with – Fatty Streak: lipid filled smooth muscle cells (usually develops a yellow-tinged
appearance in the vessel)
 Progresses to – Fibrous Plaque: beginning of progressive changes in the endothelium of vessel
o Vessels usually repair themselves after injury, but not in pt. with CAD – LDL & platelet growth
proliferate & thicken the vessel wall
 Complicated Lesion: final stage; most dangerous, continued inflammation (look at CRP to see if
those are high – inflammatory markers)
o Plaque grows, instability, ulceration & rupture
o Activation of platelet, exposed platelets cause expression of glycoprotein IIb, IIIa receptors
that bind fibrin
o Causes further platelet aggregation & adhesions
o CRP is a nonspecific inflammation marker that is increased in pt. with CAD, which can trigger
rupture of plaque in the arteries
Risk Factors for CAD
 Non-modifiable Risks:
o Age (white, middle-aged men)
o Gender (men – differs in presentation & symptoms)
o Ethnicity (AA males have a higher tendency to have HTN at a younger age)
o Family history (even with NO other risk factors, this automatically puts you at risk)
o Genetic inheritance
 Modifiable Risks:
o a. Lipids: controlled primarily by diet & medications (statins – watch for myalgia)
▪ LDL – primary target of therapy whether with diet or medications
 Target goal for LDLs: <100 || Optimal LDL with ASCVD: <70
 100-129
Near optimal/Above optimal
 130-159
Borderline High
 160-189
High
 > 190
Very High
▪ Total Cholesterol –
 <200
Desirable
 200-239
Borderline High
 >240
High (esp. with comorbidities)
▪ HDL (good cholesterol) –
 <40
Low
 >60
High
 #1 way for pt. to increase HDL levels is to exercise (high HDL levels are
desired)
▪ Triglycerides –
 <150
Normal
 150-199
Borderline High
 200-499
High
42
N418 – Exam 1
▪
 >500
Very High
 Triglyceride levels are affected a lot by sugars (unrefined/simple sugars)
For these levels to be true the pt. has to be fasting for about 12-16 hours before test
▪
▪
o
o
o
Take into account the HDL ratio to the total cholesterol & LDL levels
New Recommendations for Statins:
 People without CV disease who are 40-75 years old & have a 7.5% or higher
risk for MI or stroke within 10 years
 People with a history of MI, stroke, angina, PAD, TIA, or coronary/arterial
revascularization
 People 21 & older who have a very high level of LDL (190 or higher)
 People with Type I or II DM who are 40-75 years old
b. Blood Pressure:
▪ Controlling BP reduces SVR which reduces the workload on the heart
▪ HTN Guidelines 2014:
 No DM/CKD <150/90 (age >60) or <140/90 (age <60)
 With DM/CKD <140/90
▪ Sodium intake, diet, exercise & mediation compliance
c. Tobacco Use:
▪ Includes smokeless & regular tobacco in addition to second-hand smoke
d. Activity:
▪
o
Not just muscle building but more CV activity (3-5 times a week for 30-40 & get HR
25% above baseline)
e. Obesity:
▪ Abdominal Obesity (waist circumference, height & weight)
 Men WC: >102cm (>40in)
 Women WC: >88cm (>35in)
▪
o
BMI (height & weight)
 BMI: >30kg/m2
f. Diabetes:
▪ Type I (juvenile; insulin-dependent)
▪ Type II (non-insulin dependent; greatest population)
▪
o
HbA1C level <7% (monitors glycemic control over past 3 months)
 If a pt. with DM already has known CAD, probably want this number to be a
little lower
g. Metabolic Syndrome:
▪ Higher risk for atherosclerotic vascular disease (includes anyone with 3 or more of the
following risk factors)
Risk Factor
Defining Level
Abdominal Obesity
-Men
-Women
Waist Circumference:
> 102 cm (> 40 in)
> 88 cm (> 35 in)
Triglycerides
>150 mg/dL
HDL Cholesterol
-Men
-Women
< 40 mg/dL
< 50 mg/dL
Blood Pressure
130/85 mm Hg or greater on
consecutive measurements
Diabetes
Glucose >110
43
N418 – Exam 1
▪
o
h. Drug History:
▪ Cocaine & Crystal Meth use play a part in CVD development (esp. cocaine)
ASCVD – Arteriosclerotic Cardiovascular Disease
 Progressive atherosclerotic disorder of the coronary arteries
 Leading cause of death in the US – decreased by 31.9%
 AHA estimates that 720,000 Americans will have an MI each year & about ¼ of these die in the ED or
before reaching the hospital
 2200 Americans die of CVD each day – 1 death in every 34 seconds
Acute Coronary Syndrome (ACS)
 Acute Coronary Syndrome (ACS) is a term used to describe a spectrum of clinical syndromes
representing varying degrees of coronary artery occlusion – when you see ACS, it is either a bunch
of syndromes or they are trying to rule out
 Spectrum of Syndromes includes:
o ST elevation MI (STEMI) – ST segment has tombstone appearance
o Non-ST elevation MI (NSTEMI)
o Unstable Angina (UA)
 Etiology & Pathophysiology:
o Deterioration of once stable plaque rupture  leads to platelet aggregation  thrombus
formation (dislodged thrombus is called an emboli)
o Resulting in –
▪ Partial occlusion of coronary artery (usually produces UA or NSTEMI)
▪ Total occlusion of coronary artery (produces STEMI)

Signs & Symptoms:
o Angina Pectoris (Chest Pain)
▪
o
Severe, immobilizing chest pain usually described as
“crush” (may radiate to jaw, shoulder, back) & is
unrelieved by rest, nitro or position changes
(elephant on my chest)
 Women & DM do not present with the classical presentation as other pt. do –
women may complain of scapula pain
▪ Can be described as an uncomfortable pressure, fullness, squeezing
▪ Chest pain will NOT be reproducible by palpation (“If I touch it does it hurt?”)
SOB, DOE (dyspnea on exertion)
44
N418 – Exam 1
o
o
o
o
o
o

Severe weakness/fatigue
Lightheadedness
Diaphoresis & N/V (acute MI)
Palpitations
Moderate to severe anxiety
Ask pt. to take a big deep breath to rule out whether or not it’s actually pleuritic chest pain
Precipitating Factors of Angina:
o Physical exertion
o Temperature extremes (usually
extremely cold temps)
o Strong emotions (anxiety, fear)
o Consumption of heavy meals
(blood diverts to GI tract to digest)
o Tobacco use
o Sexual activity
o Stimulants
o Circadian rhythm pattern (based
on cortisol – increased in AM)
45
N418 – Exam 1

Unstable Angina:
o Described as chest pain that is not predictable, often occurring at rest while increasing in
frequency & severity
o Rarely sharp or stabbing, with no changes in pain level with repositioning or breathing
o Most common pathophysiology: thrombus resulting from disruption of atherosclerotic plaque
o Some blood continues to flow through affected artery, however blood flow is severely
diminished
o Pt. generally seeks medical attention, frequently fearful of MI
o Women present differently than men vs. diabetics (may just say they aren’t feeling right)
o UA pain is more severe than stable angina pain
o Requires more frequent NTG (nitroglycerin) therapy – vasodilator used for immediate
vasodilation of coronary arteries
o EKG may show ST segment depression during acute attack (ischemia)
o ST segment may return to normal or may progress to acute MI (elevation)
Acute Myocardial Infarction (AMI)
 Ischemia resulting in the death of myocardial tissue (myocardial tissue does not regenerate – you
can limit the amount of damage to the myocardium & limit progression of the infarct)
o Electrical conduction of the heart will not be the same bc of the necrotic tissues leaving the
pt. at risk for dysrhythmias
 Caused by occlusion of the coronary artery or its branches
 Irreversible myocardial necrosis (goal of treatment: time is muscle – the sooner you restore perfusion
to the coronary tissues, the less damage you have to the muscle)
 Mostly secondary to atherosclerosis (95%)
 Other causes include:
o Coronary spasm, coronary embolism, blunt trauma (cardiac contusion), cocaine use (potent
vasoconstrictor of the BV)
 Results from prolonged ischemia which evolves over time
 Myocardial tissue can be salvaged for up to 12 hours from onset of symptoms (first thing you ask
when pt. comes in with chest pain – “When did the symptoms first start?”)
 Pathophysiology:
o Infarcted area cannot conduct electrical impulses or contract
 Clinical Manifestations of MI:
o Pain – severe, immobilizing, not relieved by position changes, rest or Nitroglycerin (hallmark)


▪ Usually occurs in the early morning hours lasting >20min & is more severe than angina
▪ Diabetics have asymptomatic MI & atypical symptoms
▪ OA may experience a change in mental status (confusion), SOB, dizziness, etc.
o SNS stimulation – catecholamine release results in release of glycogen, diaphoresis &
vasoconstriction (pt. skin may appear ashen, clammy, or cool to touch)
o CV changes – initial BP & HR elevation followed by drop in BP; may hear crackles & see JVD;
may heart S3 & S4
o N/V
o Fever
The Healing Process:
o Necrotic tissue is seen on EKG as ST segment elevation and/or pathologic Q wave
o 1-14 days after MI, the beginning scar tissues is still weak & esp. vulnerable to stress/activity
o By 6 weeks, scar tissue has replaced necrotic tissue & the injured area is healed
Complications of MI:
o Dysrhythmias in 80% of MI pt. (V-Fib most often in the first four hours after onset of pain)
o Heart failure (SOB, pulmonary edema, decreased O2, tachypnea, restlessness, agitation)
o Cardiogenic shock
o Papillary muscle dysfunction (systolic murmur at apex of the heart radiating toward axilla)
o Ventricular aneurysm
o Pericarditis
46
N418 – Exam 1
Dressier Syndrome (common post-MI – fever, pleural effusion, achy joint pain; usually treated
with NSAIDs like Naproxen)
Diagnosis of AMI:
o EKG Changes (12 Lead)
▪ ST elevation (>1mm) in 2 or more consecutive leads (STEMI)
▪ ST depression (>0.5-1mm) in more than one lead (unstable angina)
o Serial Cardiac Enzyme Values (q3h x 3)
▪ Myoglobin – in all muscles
▪ CK MB – more indicative of myocardial tissues
o

▪



Troponin Levels – most indicative marker; only marker
specific to heart muscle (also elevated in sepsis, pul. HTN
or emboli, HTN, HF)
o High level of suspicion for anyone over 35 years of age who
presents with chest pain longer than 20mins & has a
history/presence of multiple risk factors
12 Lead EKG: (#1 priority with pt. presenting with chest pain)
o Central to initial risk & treatment stratification – elevated
enzymes are NOT necessary for a decision to administer
fibrinolytics or perform PCI (pt. presenting with ST elevation
requires no other clinical evidence to be sent to the cath. lab)
o Principle: ischemic/necrotic tissue does not conduct electrical
impulses normally – reperfusion dysrhythmias
Localization of Infarction:
o Septal  V1, V2
o Anterior  V3, V4
o Lateral  I, aVL, V5, V6
o Inferior  II, III, aVF
Coronary Circulation:
o Right Coronary Artery
▪ RA  RV  SA Node  AV bundle  Posterior LV
 Inferior
▪
o

If pt. has occlusion of the right coronary artery –
we would see loss of P-wave, bradycardia due to
disruption of main SA node conduction
Left Coronary Artery
▪ Left anterior descending
 Anterior 2/3 of inter-ventricular septum
 Anterior LV
 Lateral LV
 Supplies most of the left side of the heart
▪ Circumflex (circles around)
 LA
 Posterior LV
 Lateral LV
▪ Much better to have right-sided MI than left
▪ Blockage in the left main artery commonly called the “widow maker”
Relationship between LV Surface, EKG Lead & Coronary Artery:
LV Surface
ECG Leads
Artery Involved
47
N418 – Exam 1
Inferior
II, III, aVf
RCA (80-90%)
LCX (10-20%)
Infero-lateral
II, III, aVf, V5, V6
LCX
Lateral
V5,2 V6, I, aVL
LCX
Anterior
V2, V3, V4
LAD, LM
Septal
V1, V2
LAD
Antero-septal
V1, V2, V3
LAD
Posterior
V1, V2 (reciprocal)
LC or RCA

EKG Changes Associated with ACS:
o ST Segment: J point to the beginning of the T wave (J point – where QRS returns to baseline)
o Pathological Q wave is more than ½ mm deflection (deeper & taller Q waves)
o ST Segment Elevation (septal/anterior)
o aVR: if it is upright, it’s V-Tach

Cardiac Markers:
o Time Review
▪ CK (CK-MB specific for myocardium) – third to go up
 Rises at 6 hours, peaks at 18 hours, returns to normal in 24-35hrs
▪ Troponin (myocardial muscle protein)
 Rises at 4-6 hours, peaks at 10-24 hours, returns to normal in 10-14 days
▪ Myoglobin (all muscles) – first to rise
 Rises at 2 hours, peaks at 3-15 hours, returns to normal in 24 hours
 Myoglobin is rapidly excreted in the urine resulting in a rapid return to baseline
Collaborative Management/Goals:
o Reduce the amount of myocardial necrosis that occurs in pt. with MI
o Prevent major adverse cardiac events (MACE) – things like v-tach, f-fib
o Treat acute, life threatening complications
Emergency Management:
o M-O-N-A


o
▪ Morphine (vasodilator of coronary arteries)
▪ Oxygen (2-4L)
▪ Nitroglycerin
▪ Aspirin
Monitor v/s & pulse oximetry closely during the first few hours after admission
48
N418 – Exam 1
o


Bed rest & limitation of activity are initially ordered for 12-24 hours with gradual increase in
activity
Management of MI:
o Mainstay of treatment for STEMI is early reperfusion (within 12 hours of onset of symptoms) to
prevent muscle damage
▪ “Time is muscle” – the shorter the time to reperfuse the greater the benefits (47%
reduction of mortality was noted when fibrinolytic therapy was provided within the
first hour)
▪ Reperfusion therapy includes emergent PCI or fibrinolytic therapy
o UA or STEMI with negative cardiac markers & ongoing angina:
▪ Combination of aspirin, Heparin & a glycoprotein IIb/IIIa
▪ PCI considered once angina is controlled or angina returns & increases in severity
Pharmacological Treatment: (Table 34-11: p. 744)
o Beta-Blockers: typically always given
▪
▪
▪
▪
o
IV route
Contraindicated if HR <50 or SBP <90
Decreases workload of the heart
Selective Beta-Blockers:
 B1 – heart
 B2 – lungs
Morphine Sulfate:
o
▪ Good for persistent symptoms/pulmonary edema
▪ Good coronary artery vasodilator (monitor pt. for bradypnea or hypoxia)
Ca Channel Blocker:
o
▪ Given if pt. cannot tolerate beta-blocker
Nitroglycerin:
o
▪ Give this first if chest pain is unrelieved by other measures THEN give morphine
▪ Decreases angina
▪ Typically given IV
ACEI/ARB:
o
▪
▪
ASA:
o
▪ 162-325mg crush/chew
▪ Either baby aspirin or full dose Bayer aspirin given, pt. chews it & put on O2
O2 Therapy:
▪
Reduces HF – if EF <40% & SBP <100, pt. should be on ACEI/ARB
Decreases afterload
Keep sat levels >90%
Nitroglycerin
 Vasodilator of coronary & peripheral arteries – can cause hypotension
o Used to increase preload & afterload while increasing the myocardial oxygen supply
 Requires titration: keep SBP >90 (limit drop in BP to 30mmHg below baseline in HTN pt.)
 Types of Nitroglycerin:
o Short Acting: spray, tablets (keep the bottle out of light)
o Long Acting: Imdur, Isordil, Renexa
o Ointment: paste goes on white paper – changed q6h (ONLY used in hospitals)
o Transdermal Patches: 12 hours on/12 hours off (prevents NTG induced vasodilation
tolerance)
 HA is a common SIGN of NTG use, not a SE – give pt. Tylenol
49
N418 – Exam 1

There is no ceiling effect for Nitroglycerin – aka there’s no maximum dose
Fibrinolytics
 Decreases risk of thrombus formation (unstable angina means that plaque area is ulcerative 
platelets aggregate clot forms and become a thrombus)
 *Used only in ST elevation MI
 “Door to Needle”  < 30 minutes; Integrilin
 Preferable to administer within 3 hours of symptoms but can be administered up to 12 hours- that’s
why always ask when did your chest pain start
 Most reliable sign that reperfusion has taken place is ST segment returning to baseline
 Treatment with fibrinolytics is aimed at stopping the infarction process by dissolving the thrombus in
the coronary artery & reperfusion of the myocardium
 Examples of Fibrinolytics:
o Streptokinase
o Anistreplase – Eminase
o Alteplase- Activase
o Reteplase – Retavase
o Tenecteplase – TNK
 Complications of Fibrinolytics:
o Reperfusion arrhythmias (v-tach & v-fib)
o Bleeding (stop infusion & notify MD– decreased BP, increased HR, LOC or urine changes)
 Contraindications to use of Fibrinolytics:
o Absolute
▪
▪
▪
o
ICH
IC Neoplasm
Previous cerebral hemorrhage
▪ Closed head injury within 3 months
▪ Active internal bleed
▪ Suspected aortic dissection
▪ Pt. >75 or 80 years old
Relative
▪
Active PUD
▪
▪
▪
▪
▪
HTN SBP >180/DBP > 110 (can have cerebral bleed)
Ischemic CVA > 3 months
Trauma or prolonged CPR > 10min
Serious systemic disease (advanced cancer, severe liver/kidney disease)
Rectal bleed
▪
▪
▪
Pregnant
Recent surgery (last 3 weeks)
Current use of anticoagulants
Other Medications (see these used more for STEMI than NON-STEMI and unstable angina)
 Heparin (continuous drip)
o As adjunctive therapy with fibrinolytics
o With Aspirin and other platelet inhibitors in Unstable Angina and NSTEMI
 Glycoprotein IIb/IIIa Inhibitors (ReoPro [cath lab], Integrilin [before pt. goes to cath lab and
continued after on floor], Aggrastat [cath lab])
o Used with ASA, Heparin, and Clopidogrel (Plavix) and early PCI for UA/NSTEMI
 Antiplatelets after PCI (Plavix, Effient, Brilinta)
o Post stent placement* – decrease platelet aggregation until endothelial grows over stent
o Important to educate about NOT MISSING DOSES*
 Statins – usually started within 24 hours of having the diagnostic lipid panel
50
N418 – Exam 1
Taken at night, when the liver synthesizes cholesterol
New standards: if a patient comes in with an elevated lipid panel, even if they haven’t had
any s/s, they want to start them on statins
ACE Inhibitors – within 24 hours
o Recommended following anterior wall MI or MI that results in LV dysfunction or pulmonary
congestion
o Prevents ventricular remodeling & slows the progression of HF (mainstay of treatment of HF)
o Protects the kidneys (DM pt. should probably already be on this)
o Decreases peripheral vascular resistance (afterload)
o For ejection fraction <40
Beta Blockers – (OLOLs) administered in the ED as a first line for all types of ACS
o Used to decrease myocardial O2 demand by…
▪ Reducing the HR, BP & contractility (heart pumps more effectively)
o Decrease workload of the heart and decrease remodeling of the heart
o Start out on Lopressor (BID) and sent home on Metoprolol (QD)
o All pt’s that come in w/unstable angina or acute coronary syndrome get this
▪ Used in the first 24 hours of an MI to reduce the size of the infarction
o
o


Percutaneous Coronary Intervention (PCI)
 Recommended first line treatment for pt. with confirmed MI
 Performed if diagnosis of STEMI is in doubt or confirmed STEMI has occurred
 Preferred if onset of symptoms > 3h
 Skilled PCI facility with surgical back-up
 Goal is to reopen the affected artery (“Door to Balloon”) in <90mins
o From the time the pt. hits the ER (code STEMI) to open the affected artery – <90mins
o If there is doubt about whether pt. is having a STEMI or not, this is still done
o Cardiac catheterization is done first to assess location of blockage, severity, collateral
circulation & left ventricular dysfunction
o If severe left ventricular dysfunction, IAPB may also be required (or CABG)
Complications of MI
 Dysrhythmias (80%)
◦ Most common complication
◦ Life-threatening dysrhythmias occur mostly with anterior wall infarction, HF, or shock
◦ Complete heart block is seen in massive infarctions
◦ V. Fib, a common cause of cardiac death, is a lethal dysrhythmia that occurs most often in
the first four hours after the onset of pain
◦ PVCs may precede ventricular tachycardia and V.Fib


● If patient is in V.Tach, always check pulse first because it determines what tx you do
Heart Failure:
◦ If infracting on left side of heart then they will have heart failure; if the pump fails the fluid
back up- SOB, flash pulmonary edema, dec O2, tachypnea, etc.
◦ Complication that occurs because the pumping power of the heart has diminished
◦ HF occurs with subtle signs: mild dyspnea, restlessness, agitation, or slight tachycardia
● Other signs: pulmonary congestion on chest x-ray, S3 and S4, crackles, and JVD
◦ You will see more symptoms with left sided MI
Cardiogenic Shock
◦ Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe
left ventricular dysfunction
◦ Occurs less often now because of early PCI and fibrinolytic therapy
◦ High mortality rate
◦ Treatment includes aggressive control of dysrhythmia, IAPB therapy, and support of
contractility with the use of vasoactive drugs
● Balloon pump pumps the patient’s heart for them, while allowing their heart to rest
51
N418 – Exam 1
The goal of therapy is to maximize oxygen delivery, reduce oxygen demand, and prevent
complications such as acute renal failure
Papillary Muscle Dysfunction
◦ Occurs if infarcted area includes or is adjacent to the papillary muscle that attaches to the
mitral valve
● Causes mitral regurgitation, which increases blood in left atrium and decreases CO
◦ Detected by a systolic murmur at the apex of the heart radiating toward the axilla
Ventricular Aneurysm
◦ When infarcted myocardial wall becomes thinned and bulges out during contraction
◦ Besides ventricular rupture, which is fatal, ventricular aneurysms harbor thrombi that can lead
to emboli stroke
Pericarditis
◦ Inflammation of the visceral or parietal pericardium, resulting in cardiac compression,
decreased ventricular filling and emptying, and HF
◦ Occurs 2-3 days after an acute MI
◦ Characterized by chest pain that is aggravated by inspiration, coughing, and upper body
movement
◦ Pain is relieved by sitting in a forward position
◦ Auscultation reveals pericardial friction rub and fever may also be present
◦ Diagnosis is with ECG and tx includes aspirin, corticosteroids, and NSAIDs
Dressler Syndrome (common post MI*)
o Characterized by pericarditis with effusion (escaped fluid into cavity) and fever that
develops 4-6 weeks after MI or open heart surgery
o Caused by antigen-antibody reaction to the necrotic myocardial tissue
o Symptoms include pericardial pain, fever, friction rub, pleural effusion, and arthralgia
o Lab findings: elevated WBC and elevated sedimentation rate
o Tx: short term corticosteroids (usually treated with NSAIDs like Naproxen)
◦




Other Causes of Non-Cardiac Chest Pain
 Pulmonary
o PNA
o Pleuritis
o Pneumothorax
o Pulmonary Embolus- if pt. has chest not relieved with nitro, cardiac enzymes not elevated,
they will rule out PE
o Pulmonary HTN
 GI Causes
o Reflux
o Esophageal spasm
o PUD
o Pancreatitis
 Musculoskeletal and Misc.
o Chostochondritis
o Herpes Zoster (shingles)
o Anxiety
▪ Pericarditis, heart failure, etc.
Angiograms
 Right side: venous circulation and looks at right sided heart pressures, access a vein
 Left side: evaluates coronary arterial blood flow. To see if pt has blockage. Access an artery. Will be
given dye (can effect the kidneys, pt needs to be well hydrated)
****Review Fig. 34-5 on p. 743 – Collaborative care: chronic stable angina & acute coronary syndrome
52
N418 – Exam 1
53
N418 – Exam 1
(6) CARDIAC REPERFUSION: PCI & CABG
Cath Lab Report
Coronary Angiogram
 Diagnostic study
 Puncture Sites
 Right vs. Left Heart Cath
o Right cath – venous access through inferior vena cava
into the RA to insert PA catheter to obtain pressures
o Left cath – accessed through femoral or radial artery &
fed through vessels until it reaches the aorta; die is then
injected
o Left ventriculogram – provides information about the EF%
o To obtain an EF%, both right & left heart cath will need to
be performed
o Radial stick (easier pt. recovery)
o Brachial approach is also an option
o Most common approach is through the femoral artery
 Contrast Dye (will feel warm sensation; pt. allergy to shellfish requires notification of MD)
o Contrast dye is nephrotoxic so if pt. has renal insufficiency ensure pt. is well hydrated & limit
the use of dye as much as possible (typically give 1-2L of NS after procedure)
o Use Mucomyst to prevent reactions
 Assessment (same as PCI) – pedal pulses, V/S, BP, HR, monitoring of puncture site
Percutaneous Coronary Intervention (PCI)
 Done in cath lab
 Less invasive & less recovery time than surgery (PCI is NOT a
surgical procedure)
 Types of PCI:
o Balloon angioplasty (high pressure balloon opens up
vessel – coronary artery)
o Stent placement (not done unless blockage is 60-70% or
greater)
o Atherectomy (sucks plaque out of vessel)
 Successful PTCA:
o Stretches vessel wall, fractures plaque & enlarges the
vessel lumen
o Reduces stenosis to <50% of the vessel lumen diameter
90% of the time (goal is to restore circulation)
o Restenosis occurs in more than 1/3 of pt. during the first
year (due to platelet-mediated intimal hyperplasia)
o Pt. should NOT have chest pain after procedure
 Complications of PCI:
o Dissection of dilated artery (can lead to cardiac
tamponade, ischemia & infarct)
o Plaque embolus (can lead to MI)
o Coronary spasm (prevented through injection of intracoronary Nitroglycerin to dilate the artery)
o Spontaneous restenosis
o CABG required for 3-4% of PCI pt.
Balloon Angioplasty
Atherectomy
 Removal of plaque by excision
 Uses a rotational blade to shave plaque off
 Less incidence of abrupt closure when compared to PCI
 Limited to select location(s) of lesion in the artery (performed on distal vessels – NOT done high on
the LAD bc this would place pt. more at risk for an emboli)
54
N418 – Exam 1
Coronary Stents
 Placement during PCI
 Reduces restenosis rate of PCI
 Two types of stents:
o Bare metal
o Drug-eluding (chemotherapy type agent proven
to prevent re-stenosis – pt. usually on anti-plaelets
for 6 months-1 year)
Coronary Artery Stent
Nursing Management Post-PCI
 Monitor for chest pain & ST segment changes (possible
signs of acute closure)
 Monitor vital signs (sudden drop in BP might indicate that pt. is “vagaling” or bleeding from the
femoral artery)
 Monitor groin site (distal pulses, HR & BP, bleeding – bed rest for 4-6 hours)
 Monitor anticoagulant or antiplatelet drips – bleeding (Integrillin, Aggrestat, Angiomax)
o These medications prevent platelets from aggregating on the new stent
o Angiomax (anticoagulant) – have to wait 2 hours before pulling sheath if this med is used
 Monitor vasodilator drips (Tridil – Nitroglycerin)
 Administer oral antiplatelet medications (Plavix, Effient, ASA)
o Plavix: usually given as a bolus in cath lab – given for CVA, stent, or circulatory issues

▪ Bare metal stent requires pt. to be on Plavix for about 6 months
▪ Drug-eluding stent or saphenous vein graft pt. will be on Plavix for life
o Effient: only used for stents
o ASA: will be started within 24 hours
Managing the vascular access site
o Monitor for bleeding & check the distal pulses
o Instruct pt. to keep leg straight & head down
o HOB should remain flat when sheath is in place (when pulled, apply direct pressure for 10-15
minutes)
o Assess for hematoma (painful “egg” underneath skin – very painful & throbbing)
o Closure devices (Angio-seal, Perclose – suturing of artery, Starclose)
Starclose
Angio-seal
Femoral Artery Closure Devices
55
N418 – Exam 1
Discharge Instructions Post-PCI/Angiogram
 Keep incision site clean & dry (NO ointments, powders, or peroxide)
 Activity level (no lifting over 5lbs – activity is limited for a week)
 Medication teaching –
o Oral Antiplatelet: Plavix, ASA daily
o Beta-Blockers: slows HR down if MI occurred
o Ca Channel Blockers: reduces workload of heart & used for vasospasms
o Nitrates: reduces incidences of angina attacks – this is long-acting Nitrates like Imdur
 What to watch for! o Chest pain or SOB
o Bleeding or swelling at insertion site (lay flat, hold pressure, call 911)
o Pain at insertion site (possible hematoma – dropping BP or severe back pain are signs of a
retroperitoneal bleeding issue diagnosed with CT scan)
o Feeling faint or weak (signs of possible internal bleeding)
o Signs of infection (redness, drainage, fever)
Coronary Artery Bypass Graft (CABG)
 Open heart surgery in which a prosthesis or a section of a blood vessel is grafted onto one of the
coronary arteries bypassing a narrowing or blocking in a coronary artery
o Have been performed since the 1960s
o Overall mortality is 1-3%
o Performed on-pump OR off-pump
 Advantages over PCI:
o Provides more complete revascularization & shows better long-term relief of symptoms
o Less than 10% of pt. need subsequent revascularization within 5-7 years
 Disadvantages compared to PCI:
o More procedural related pain
o Longer hospital stay
o More procedural infarctions
 Indications for CABG:
o For pt. with mild or no symptoms –
▪ Significant left main coronary stenosis
o
▪ Significant (>70% of LAD & LC)
▪ Three Vessel Disease
For pt. with stable angina –
▪ Significant left main coronary stenosis
▪ Significant (>70% of LA & LC)
▪ Three Vessel Disease
▪
o
o
Two vessel disease with significant proximal LAD stenosis & EF <50% or demonstrable
ischemia on non-invasive testing
For pt. with unstable angina/NSTEMI –
▪ Significant left main coronary stenosis
▪ Significant (>70% of LA & LC)
▪ When percutaneous revascularization is not possible
▪ When ischemia is not responsive to maximal non-surgical treatment
For pt. with STEMI (Urgent CABG) –
▪ Failed angioplasty with persistent pain
▪ Persistent or recurrent ischemia refractory to medical therapy
▪ When percutaneous revascularization is not possible
▪
▪
When ischemia is not responsive to maximal non-surgical treatment
Cardiogenic shock in pt. <75yo with ST elevation (may stay on balloon pump after)
56
N418 – Exam 1
▪
Life threatening ventricular arrhythmia in the presence of >50% of left main stenosis
and/or triple vessel disease
 V-Tach  check pulse first
 V-Fib  defibrillate first
Minimally Invasive CABG
Cardiac Surgery
 Typically the saphenous vein or internal mammary artery is
used to bypass a stenotic lesion
 Often requires cardiopulmonary bypass (CPBP)
 Off pump CAB (full or partial sternotomy on a beating heart)
 Minimally invasive CABG –
o Used for LAD or single vessel disease
o Several small thoracic incisions made
o LIMA is accessed & heart is slowed with Beta-Blocker or
Ca Channel Blocker
o LIMA is used to bypass LAD lesion
o Done through specialized scopes & camera in which
the surgeon dissects the internal mammary artery &
bypasses it
Saphenous Graft
Internal Mammary Graft


Post-op Care:
o Usually taken directly to ICU (usually stays here 24-36 hours)
o Nurse should receive report (summary of surgery, “pump time”, IV running, recent lab values
including ABGS)
o Pt. is initially intubated (goal is to extubate pt. 4-6 hours after getting to ICU)
o PA line
o Arterial line
o Pacer wires
o Multiple IVs
o NG tube
o Chest tubes (medistinal & pleural)
Nursing Assessment:
o Vital signs
o Hemodynamic status
▪ Ex: pt. comes back with elevated PAP & PAWP – will probably need positive inotropes
to increase CO bc these elevations mean the LV is not working
▪ Ex: pt. comes back with low CVP & urinary output – will probably need crystalloids or
colloids (or blood products if H&H is low)
o O2 saturation, ABGs, ventilator settings
57
N418 – Exam 1
o
o
o
o
Electrolytes, CBC
Chest tube drainage
Urine output
Neurologic complications (post-cardiotomy delirium; intraoperative CVA or MI)
Nursing Management Post-Cardiac Surgery
 Normalize cardiac output (CO) –
o Optimize HR (temporary pacing, drug therapy)
o Achieve normal CO through drug therapy & volume replacement – use temporary pacing if
HR becomes a problem
 Monitor for dysrhythmias – (esp. ventricular)
o Watch for A-Fib (occurs in 20-40% of pt.) – frequent PAC typically indicates a pt. that is about
to go into A-Fib
▪ Monitor the pt. rate more than the rhythm with A-Fib – occurs more often 2-3 days
post-op when they start ambulating
▪ Treat with Amiodarone & Ca Channel Blocker (go home on these for 3 months)
 Manage preload –
o Administer volume as needed for low PAWP/CVP (crystalloids, colloids, packed RBCs)
o Albumin is another option to increase preload
o Diuretics can be given as needed
 Manage Hypokalemia (dec. K) –
o Causes of Low Potassium loss of reabsorption due to administration of Lasix, Bumex
o Concentration of IV K solution does not exceed 20mEq/100mL when administered on a
regular nursing floor or 40mEq/100mL in the ICU or telemetry units
o Maximum administration rate < 20mEq/hr
o Daily dose may not exceed 200mEq/day
 Manage Hyperkalemia (inc. K) –
o Stabilize myocardial cell membrane:
▪ Ca Chloride (10%): 5-10mL (500-1000mg) IV over 2-5 minutes
▪ Ca Gluconate (10%): 15-30mL IV over 2-5 minutes
Shift K into cells:
▪ Sodium bicarbonate: 50 mEq IV over 5min
▪ Glucose plus insulin: mix 25g (50mL of D50) glucose & 10 U regular insulin & give over
15-30 min
▪ Nebulized albuterol: 10-20mg nebulized over 15min
o Promote K excretion:
▪ Diuresis: achieved by administration of furosemide (Lasix) 40-80mg IV
▪ Kayexalate: 15-50g plus sorbitol PO or rectally
▪ Dialysis
Manage afterload –
o Increased SVR & HTN commonly occurs after surgery (due to effects of hypothermia)
▪ Can exacerbate bleeding & increase LV workload
o Control HTN (Nipride, NTG, anti-hypertensive medications)
o Decreased SVR through vasodilation
Manage contractility –
o Positive inotropes (Dopamine, Dobutamine, Primacor)
o IABP (only used to give heart time to rest if pt. doesn’t respond to inotropes)
Control bleeding complications –
o More than 150mL/hr requires intervention (clotting factors, protamine sulfate, blood
replacement based on loss & Hct values)
o



58
N418 – Exam 1
Assess for cardiac tamponade (low BP, JVD, sudden cessation of chest tube drainage, PEA
 requires emergency sternotomy)
Prevent infection (important to maintain a normal glucose level) –
o Operative wound infection
o Infective endocarditis
o Pneumonia (early ambulation)
o UTI
Preserve renal function –
o Hemolysis caused by pump may damage renal tubules leading to ARF caused by
decreased renal perfusion
o Vigilant monitoring of urine output, electrolytes, BUN & Creatinine (ratio 10:1/20:1)
▪ BUN is more affected by dehydration (will be elevated)
▪ Creatinine is a truer indication of renal function
o Maintain adequate hydration & preload (administer diuretics as needed)
o Monitor daily weights
Outcomes:
o Extubation ASAP
o PA catheter is usually removed on post-op day 1
o Out of bed & to a chair on post-op day 1
o Out of ICU on post-op day 1-2
o Home in 4-5 days if uncomplicated (average stay is 5-7 days)
Discharge:
o Aspirin (baby aspirin)
o Beta-Blockers
o ACE Inhibitors
o Statins
o Pain medications
Patient Teaching:
o Limit use of arms in addition to gradually increasing activity level
o Wear TED hoses, continue incentive spirometer, elevate legs for edema, SHOWERS
o





Research
 Stem cell injection after AMI to stimulate new growth of myocardial cells
 Gene therapy for chronic CAD to stimulate angiogenesis (growth of new vessels)
59
N418 – Exam 1
DYSRHYTHMIAS – SVT, PVCs & A-Fib
Dysrhythmias
 Abnormal cardiac rhythms are termed dysrhythmias
 Prompt assessment of dysrhythmias & the pt. response to the rhythm is critical
Evaluation of Dysrhythmias
 Regular EKG monitoring
 Holter monitoring:
o External box that records a 24-hour EKG tracing (pt. keeps daily activity diary)
 Event recorder monitoring:
o Pt. activates recorder during periods of lightheadedness or chest pain
o Basically a high-tech Holter
 Exercise treadmill testing:
o Performed to elicit dysrhythmias
o If pt. is unable to physically do this, perform a cardiolight stress test (pt. is given a substance
like Adenosine to stimulate their heart & see what the EKG reads)
 Signal EKG:
o Does NOT allow for all views of the heart
o Provides a one time snap-shot of dysrhythmia
 Serial 12-Lead EKG (always compare to a previous lead)
 Electrophysiological (EP) study:
o Performed by specialized cardiologist in cath lab (venous access also looks at pressures)
o Stimulate the pt. to go into an arrhythmia by introducing different catheters
o Used to identify focal points of irritability/re-entry & can evaluate effectiveness of drugs
o Very time-consuming study
Sinus Tachycardia
 Discharge rate from the SA node is increased as a result of vagal inhibition
o Rate is >100 bpm
o Sinus tachycardia will NOT have a rate >140-150 bpm
 Clinical Associations: (physiological stressors)
o Exercise
o Pain
o Hypovolemia
o MI
o Heart failure
o Fever, infection, thyroid disorders
 Clinical Significance:
o Dizziness & hypotension due to decreased
CO
o Increased myocardial O2 consumption may cause angina
 Treatment: (treat the cause)
o Beta-blockers (reduce HR & myocardial O2 consumption - Lopressor)
▪
o
o
If sinus tach is due to MI or other disease processes, we treat it with beta-blockers –
decreases sympathetic system stimulation & reduces work load of the heart with the
ultimate goal of decreasing HR
▪ Beta-blocker act as a negative chronotropic (decreases rate)
Antipyretics to treat fever
Analgesics to treat pain
Beta-Blockers (3 Classes)
 Non-selective Beta-Blockers: stimulates both beta-1(heart) & beta-2 (lungs)
o Propranolol (Inderal)
o Sotalol (Beta-pace) – pro-dysrhythmic
60
N418 – Exam 1


Cardioselective Beta-Blockers: beta-1  doesn’t cause issues in pt. with pulmonary conditions
o Atenolol (Tenormin)
o Acebutolol (Sectral)
o Metoprolol (Lopressor, Toprol XL)
o Bisoprolol (Zebeta)
o Esmolol (Brevibloc)
o Nebivolol (Bystolic)
Combination Alpha [peripheral] & Beta-Blockers: decreases both BP & HR
o Labetalol (Trandate)
o Carvedilol (Coreg)
Potassium Channel Blockers
 Anytime a pt. is started on a new anti-arrhythmic drug, they need to be monitored in a hospital
setting even though they are not physically ill – antidysrhythmic medications are “pro-dysrhythmia”
meaning they are used to treat dysrhythmias BUT they can also cause dysrhythmias
 Amiodarone (Cordarone)
o Most widely used K-channel blocker; used for atrial & ventricular dysrhythmias
 Azimilide (Stedicor)
 Dofetilide (Tikosyn) – pro-dysrhythmic
o Obtain 12-lead EKG readings & monitor the QT interval – QT interval determines dosing
 Ibutilide (Corvert)
o Temporarily puts pt. in asystole
Vaughan Williams Classification of Antiarrhythmic Drugs
 Class I: Sodium-Channel Blockers (atrial & ventricular) – most cardiotoxic group
o IA: moderately slow conduction, moderately prolonged duration of action potential
▪ Ex: Qunidine, Procainamide, Disopyramide
o IB: minimally slowed conduction, shortened duration of action potential
▪ Ex: Lidocaine, Mexiletine, Tocainamide, Phenytoin (Dilantin)
o IC: markedly slowed conduction, minimally duration of action potential
▪ Ex: Flecainide, Encainide, Propafenone, Moricizinze
 Class II: Beta-Blockers (active in AV nodes, ventricles)
o Virtually no pro-arrhythmic effects
 Class III: Potassium-Channel Blockers (prolonged duration of action potential)
 Class IV: Ca Channel Blockers (active in AV nodes)
o Virtually no pro-arrhythmic effects
Premature Atrial Contraction (PAC)
 Contraction originating from ectopic focus in atrium in location other than the SA node
 Impulse travels across atria by an abnormal pathway, creating a distorted P-wave
 May be stopped, delayed, or conducted normally at the AV node
 Can be pointed – these early P-waves make the rhythm irregular
Premature Atrial Contraction (PAC)
o
o
o
 Clinical
Associations:
o Emotional
stress
o Use of
caffeine,
tobacco,
alcohol
Hypoxia (PACs are common with decreased oxygenation – COPD pt.)
Electrolyte imbalances (Potassium K & Magnesium Mg)
COPD
61
N418 – Exam 1


o Valvular disease (mitral valve prolapse)
Clinical Significance:
o Isolated PACs are not significant in those with healthy hearts – typically don’t even know
they’re having them
o In pt. with heart disease, may be a warning of more serious dysrhythmia
▪ Absolute Refractory: something can hit on T wave & nothing happens
▪ Relative Refractory: if something hits the T wave, it can stimulate a dysrhythmia
▪ More frequent PACs are more likely to cause a pt. to go into atrial fibrillation (A-Fib)
Treatment: depends on symptoms
o b-Adrenergic Blockers used to decrease PACs
▪
o
This treatment regimen usually not done unless pt. has a co-morbidity in which they
need to be on the beta-blocker anyway
▪ Use selective beta-blockers if pt. also has COPD; use non-selective without COPD
Reduce or eliminate caffeine
Paroxysmal Supraventricular Tachycardia (PSVT)
 Originates in ectopic focus anywhere above the bifurcation of Bundle of His
 Run of repeated premature beats is initiated & is usually a PAC – followed by run of narrow QRS
 Paroxysmal refers to an abrupt onset & termination
 Some degree of AV block may be present
 Can occur in Wolff-Parkinson-White syndrome (WPW) – tachycardia unresponsive to drugs
Paroxysmal SVTs


Clinical Associations:
o In a normal heart  overexertion, emotional stress, stimulants – palpitations & SOB
o Digitalis toxicity (Digoxin slows the HR – also a pro-dysrhythmia)
o Rheumatic heart disease
o CAD
o Cor pulmonale (same is right-sided HF)
Clinical Significance:
o Depends on the pt. predisposing condition before
o Prolonged episode & HR >180bpm may precipitate decreased CO
▪ Palpitations
▪ Hypotension
▪ Dyspnea
▪ Angina
▪
▪

Dizziness
Discomfort
Treatment:
o Vagal maneuvers such as valsalva, coughing, carotid stimulation [not within our scope]
o IV Adenosine (Adenocard) – also for WPW syndrome
▪
Very short-acting drug available in a prefilled syringe
▪
▪
▪
Pt. should be placed on telemetry monitoring
Access through antecubital two-port IV site (flush in one, adenosine in other)
Administer Adenosine, flush, then elevate the arm
62
N418 – Exam 1
o
o
If vagal maneuvers and/or drug therapy is ineffective and/or pt. becomes hemodynamically
unstable, DC cardioversion should be used
▪ Cardioversion is synchronized on R wave (pt. should be sedated)
If PSVT recurs in pt. with WPW syndrome, they may ultimately be treated with radiofrequency
catheter ablation of the accessory pathway
▪ If ectopic area is caused through a re-entrant pathway, they may ablate or burn this
pathway to try & stop this rhythm
▪ Procedure is performed in the cath lab
Junctional Dysrhythmias
 Dysrhythmia that originates in area of AV node
o P wave is embedded in the QRS complex (no atrial conduction to assist with CO)
o Can occur after QRS, in the QRS or not seen at all
 Junctional escape rate  40-60bpm
 SA node has failed to fire or the impulse has been blocked at the AV node (absent P-wave)
o When the junction failed the ventricle takes over (20-40 bpm)
o Junctional Tachycardia: same thing except rate is over 60 bpm)
Junctional Dysrhythmias



Clinical Associations:
o CAD, HF, Cardiomyopathy
o Electrolyte imbalances (K & Mg – rule of thumb is to always give your Mg first)
o Inferior MI (inferior lead is associated with RCA – blocks out flow to the atrium)
o Rheumatic heart disease
o Drugs: Digoxin, amphetamines, caffeine, nicotine
Clinical Significance:
o Serves as safety mechanism when SA node has not been effective
o Escape rhythms should NOT be suppressed
o If rhythms are rapid, may result in reduction of CO & HR
▪ SOB, lightheadedness, dizziness
Treatment:
o If symptomatic, treat with Atropine
o
o
o
▪ Dose for symptomatic bradycardia – 0.5mg [1/2amp]
If accelerated junctional rhythm & junctional tachycardia is being caused by Dig toxicity,
hold the next dose of Digoxin
Beta-blockers, Ca Channel Blockers & Amiodarone used for rate control for junctional
tachycardia NOT caused by digoxin toxicity
Contraindications: DC Cardioversion
Ca Channel Blockers
 Amlodipine (Norvasc)
 Clevidipine (Cleviprex) – ONLY in ICU
 Diltiazem (Cardizem)
 Felodipine (Plendil)
 Isradipine (Dynacirc)




Nifedipine (Adalat, Procardia)
Nicardipine (Cardene)
Nislodipine (Sular)
Verapamil (Calan, Isoptin)
63
N418 – Exam 1
Remember  SVT is a narrow QRS & V-Tach is a wide QRS
Premature Ventricular Contractions
 Contraction originating in ectopic focus of the ventricles
 Premature occurrence of a wide & distorted QRS complex
o Unifocal – comes from same area of irritability – better
than multifocal
o Multifocal – comes from different areas of irritability
o Bigeminy – every other beat
o Trigeminy – every third beat
o Couplets & Triplets – typically from the same area of
irritability
▪ More than 3 PVCs are considered run of V-Tach
R-on-T Phenomena – monitor for this when the QRS
complexes are coming closer & closer to the T wave
Clinical Associations:
o Stimulants (caffeine, alcohol, nicotine, aminophylline, epinephrine, Adderall)
o Digoxin
o Electrolyte imbalances (hypokalemia)
o Hypoxia
o Fever
o Disease states: MI, mitral valve prolapse, HF, CAD
Clinical Significance:
o Usually benign in a normal heart
o In pt. with heart disease, PVCs may decrease CO & precipitate angina & HF
▪ Pt. response to PVCs must be monitored
▪ PVCs often do not generate a sufficient ventricular contraction to result in a
peripheral pulse
▪ Apical-radial pulse rate should be assessed to determine if a pulse deficit exists
o Represents ventricular irritability
▪ Can be from a clot, CAD with blockage, ischemia, etc.
o May occur –
▪ Lysis of coronary artery clot w/ thrombolytic in acute MI (reperfusion dysrhythmias)
▪ Following plaque reduction after PCI
Treatment:
o Based on cause of PVCs –
▪ Oxygen therapy for hypoxia
▪ Electrolyte replacement
▪ Drugs: Beta-blockers, Procainamide, Amiodarone, Lidocaine
o



Ventricular Tachycardia (V-Tach)
 Run of three or more PVCs
 Monomorphic, polymorphic (Torsades de Pointes), sustained or non-sustained
 Considered life-threatening because of decreased CO & the possibility of deterioration to V-Fib
64
N418 – Exam 1
V-Tach


 Clinical
Associations:
o MI, CA,
Cardiomyopathy
o Electrolyte imbalances (hypomagnesemia – biggest cause of Torsades de Pointes)
o Mitral valve prolapse
o Long QT syndrome (antibiotics, cancer drugs, cardiac drugs, N/V, antipsychotics, TCAs)
o Digitalis toxicity
o CNS disorders
Clinical Significance:
o VT can be stable or unstable (pulseless)
o Sustained VT can result in a severe decrease in CO
▪ Hypotension
▪ Pulmonary edema
▪ Decreased cerebral blood flow (changes in LOC)
▪ Cardiopulmonary arrest
o Treatment for VT must be rapid & may recur if prophylactic treatment is not initiated
o V-Fib may develop
Treatment:
o Precipitating causes must be identified & treated (ex: hypoxia)
o Monomorphic VT –
▪ Hemodynamically stable + preserved LV function:
 IV Procainamide, Sotalol, Amiodarone
▪
o
o
Hemodynamically unstable or poor LV function:
 Amiodarone followed by cardioversion (wide & regular)
 Monitor for SE of Amiodarone  pulmonary toxicity & thyroid problems
Torsades de Pointes –
▪ Polymorphic VT with changing back & forth shape, size QRS:
 IV Magnesium (treatment of choice)
 Phenytoin (Dilantin)
 Antitachycardia (Override) Pacing
▪ Drugs that prolong the QT interval should be D/C
▪ If rhythm is not converted, cardioversion may be needed
Pulseless V-Tach –
▪
▪
▪
This is a life-threatening situation (CPR, defibrillate, Epi + Amiodarone)
Requires CPR & rapid defibrillation
Epinephrine (1mg q3-5min) administered if defibrillation is unsuccessful
Ventricular Fibrillation (V-Fib)
 Severe derangement of the heart rhythm characterized on EKG by irregular undulations of varying
contour & amplitude
 No effective contractions or CO occurs
 Can have either coarse or fine V-Fib – both the same
65
N418 – Exam 1



Clinical Associations:
o Acute MI, CAD, cardiomyopathy
o May occur during cardiac pacing or
cardiac catheterization (PCI)
o May occur with coronary reperfusion
after Fibrinolytic therapy (reperfusion
dysrhythmias)
o Accidental electrical shock
o Hyperkalemia
o Hypoxia
o Acidosis
o Drug toxicity
V-Fib
Clinical Significance:
o Unresponsive, pulseless & apneic state
o If V-Fib is not treated rapidly, death will result
Treatment:
o Immediate initiation of CPR & ACLS measures with the use of defibrillation & definitive drug
therapy
o Goal is to immediately shock – start CPR until the AED arrives (compressions are better than
ventilation)
Asystole
 Represents total absence of ventricular electrical activity (FLAT LINE)
 No ventricular contraction (CO) occurs because depolarization does not occur
 If pt. is in asystole:
o First thing we do is assess – the lead wires could be off
o Check & make sure the asystole is occurring in two leads for confirmation
 Clinical Associations:
o Advanced cardiac disease (multiple MI or blockage)
o Severe cardiac conduction system disturbance (PVCs, V-Tach)
o End-stage HF
 Clinical Significance:
o Unresponsive, pulseless & apneic state
o Prognosis for asystole is extremely poor
 Treatment: (CPR  intubation  Epi + Atropine)
o CPR & initiation of ACLS measures (intubation, transcutaneous pacing & IV epinephrine)
Pulseless Electrical Activity (PEA)
 Electrical activity can be observed on the EKG, but there is no mechanical activity of the ventricles
& the pt. has no pulse
 Any rhythm (besides V-tach & V-fib) that does NOT have a pulse
 Clinical Associations:
o Hypovolemia (administer fluids)
o Hypoxia
o Metabolic acidosis
o Hyperkalemia or hypokalemia
o Hypothermia
o Drug overdose
o Cardiac Tamponade (drain fluid or assist with pericardial tap)
o MI
o Tension Pneumothorax (assist with chest tube insertion)
o Pulmonary embolism
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N418 – Exam 1

Treatment:
o CPR followed by intubation & IV epinephrine (only if ventricular rate is slow)
o If pt. presents with sinus tachycardia PEA – do NOT give pt. epinephrine
o Treatment is directed toward correction of the underlying cause
Sudden Cardiac Death (SCD)
 Death from a cardiac cause (usually an MI)
 Majority of SCDs result from ventricular dysrhythmias
o V-Tach
o V-Fib
 Goal is to perform chest compressions over ventilations
Prodysrhythmia
 Clinical Significance:
o Antidysrhythmic drugs may cause life-threatening dysrhythmias
o Risk increases in the presence of –
▪ Severe LV dysfunction (abnormal CO & EF <40% 
usually previous MIs)

▪ Digoxin & class IA, IC & III antidysrhythmia drugs
Treatment:
o First several days of drug therapy are the vulnerable
period for developing pro-dysrhythmias
o Many PO anti-dysrhythmia drug regimens are initiated &
monitoring in a hospital setting
Synchronized Cardioversion
 Choice of therapy for hemodynamically unstable, ventricular or
supraventricular tachy-dysrhythmias
o Synchronized circuit delivers a countershock on the R-wave of the QRS complex
o Synchronizer switch must be turned on
Implantable Cardioverter-Defibrillator (ICD)
 Accomplishes the same thing as if we would defibrillate the pt. – done internally
o Used for v-tach dysrhythmias
 Appropriate for pt. who –
o Have survived SCD
o Have spontaneous sustained V-Tach
o Have syncope with inducible V-Tach or V-Fib during EPS
o Are at high-risk for future life-threatening dysrhythmias
o Ischemic cardiomyopathy
o Ex: pt. with life-vest
 Consists of a lead system placed via subclavian vein to the endocardium (can be placed in the
abdomen)
o Battery-powered pulse generator is implanted Sub-Q
 ICD sensing system monitors the HR & rhythm to identify V-tach or V-fib
o Approximately 25secs after detecting V-tach or V-fib the ICD delivers <25J
o If the first shock fails, ICD delivers successive shocks
o The sensing system is done by “time”
 ICDs are equipped with antitachycardia (override paces) & antibradycardia pacemakers
o Initiates overdrive pacing of SVT & V-tach
o Provides backup pacing for bradydysrhythmias that may occur after defibrillation discharges
 Education is extremely important – variety of emotions are possible:
67
N418 – Exam 1

o Fear of body image changes
o Fear of recurrent dysrhythmias
o Expectation of pain with ICD discharge (should NOT feel pain/shock – call MD if pt. does)
o Anxiety about going home
o Anxiety about being shocked
Participation in an ICD-support group should be encouraged
Catheter Ablation Therapy
 Electrode-tipped ablation catheter “burns” accessory pathways or ectopic sites in the atria, AV
node & ventricles (venous access)
 Performed in the cath lab for pt. who have experienced treatment failure with pharmacologic
management – done to treat signs & symptoms
 Non-pharmacological treatment for –
o AV nodal reentrant tachycardia
o Reentrant tachycardia r/t accessory bypass tracts
o Control of ventricular response of certain tachydysrhythmias


Complete ablation of the AV node or bundle of His may be performed in some cases of…
o Uncontrolled ventricular response in A-fib or A-flutter that is unresponsive
o Permanent pacemaker is required
Care for Ablation Therapy:
o Not able to drive because of rotation
o Lead wires are cork-screwed into the myocardium (could cause rupture)
o Pt. Education:
▪ No bending or lifting
▪ Use dial soap
▪
▪
No bras
No high-frequency studies (cannot have MRI)
Syncope
 Brief lapse in consciousness accompanied by a loss in postural tone (AKA fainting)
 CV Causes:
o Neuro-cardiogenic Syncope or “Vasovagal” Syncope (carotid sinus sensitivity)
▪ Often a pt. will tell you they were on the toilet – “bearing down”
o Primary cardiac dysrhythmias (tachycardia, bradycardia)
▪ Tachycardia decreases perfusion to cerebral area
▪ Bradycardia does not create enough perfusion
▪ Prosthetic valve malfunction, pulmonary emboli & HF
 Non-CV Causes:
o Hypoglycemia (pt. presents with stoke-like symptoms – confusion, slow speech, sweaty)
o Hysteria/stress
o Unwitnessed seizure
o Vertebrobasilar TIA (slurred speech, face droops – lasts <24 hours)
o Dehydration
o Standing for prolonged period of time
o Carotid blockage
 Diagnostic Studies:
o Echocardiography (assess for structural deficits)
▪ Assessing for things like <EF, hypertrophy, valvular dysfunction, clots, abnormal
pressures, left-or-right-sided HF
▪ Echo with Bubble Study: seeing if deoxygenated blood crosses over to the other side
of the heart without going through the lugs
▪ Transthoracic Echo: Dopplar study
68
N418 – Exam 1
o
▪
Transesophageal Echo: probe is sent down pt. esophagus
▪
Re-introducing the tachyarrhythmia to see if it is a re-entrant pathway
EPS
▪ Performed before an ablation is done
Head-upright Tilt Table Testing
▪ Abrupt position changes to see how the vasoconstriction system reacts
▪ Performed along with EKG
o Holter Monitor
o Sub-Q implanted loop recording device (records only some of the electrical activity)
1-year mortality rate as high as 30% for syncope from CV cause
o

Loop Recorders
 Single lead EKG monitoring device
 Placed left parasternal region
 Used: diagnosis, cardiac issues for palpitations,
69
N418 – Exam 1
Atrial Arrhythmias
Atrial Arrhythmias
 Any alteration in heart rate, heart rhythm, or conduction.
 Always control the rate before the rhythm (unless it is a life-threatening rhythm)
 Many causes:
o Myocardial Ischemia is the most common—we worry about this with ACS
o Hypoxemia seen in HF (atrial fibrillation is very common in heart failure)
o Post surgery
o Heart Failure
o Stimulants
o Medications
o Hyperthyroidism, dehydration
Atrial Fibrillation
 Total disorganization of electrical activity in the atrium resulting in effective contraction
o Considered a supraventricular arrhythmia that is usually very rapid if new in onset
 Rather than an organized contraction, there is a quivering motion in atria
o Results in no movement of blood due to lack of contraction (stasis in the atria)
 Most common arrhythmia in the US & Canada
 Classification of A-Fib:
o Lone (caused by medication or stimulation – just an episode of A-fib)
o Paroxysmal (lasts 7 days or less – self-limiting A-fib requiring no medical management)
o Persistent (requires medical management – lasts longer than 7 days)
o Permanent (unresponsive to cardioversion – control is no longer being pursued)
o Continuous or intermittent
 Causes of A-Fib:
o Precursor to A-Fib is PACs – induction of A-Fib by a premature atrial beat originating in the
orifice of one of the pulmonary veins
o Underlying heart disease such as –
▪ CAD, HF, rheumatic heart disease
▪ Cardiomyopathy, pericarditis, HTN, COPD
 Hemodynamic Consequences of A-Fib:
o Atrial kick is lost resulting in a 25-30% reduction of ventricular filling  decreased CO of 20%
▪
o

Recurrent A-Fib: pt. will say that know when they are in this rhythm due to their ability
to do things (activity intolerance)
▪ Pt. with underlying CAD that goes into A-Fib will cause a faster progression to V-Fib
due to the diseased heart
Risk of thromboembolism & therefore a risk of stroke
▪ Blood remains stagnant in the atrium due to ventricular emptying
▪ Pt. with A-Fib are 2-3 times more likely to suffer a stroke
EKG Changes with A-Fib:
o Rate – new onset is usually 100-160 bpm (if medicated <100)
o Rhythm – irregularly irregular
o P wave – absent; fibrillatory/flutter waves (f) are seen (300-600/min)
o PR interval – absent
o QRS – normal (problem is above the ventricle)
o A:V Conduction – random; there isn’t a P wave for every QRS complex
70
N418 – Exam 1
A-Fib
Atrial Flutter
 Better organized in a saw-toothed pattern
o Usually the conduction ratio is normal (ex: 4 flutter waves to 1 QRS) – makes the rate regular
o Differentiation between A-fib & A-flutter depends on the conduction ratio
 Clinical presentation & management are the same as A-Fib
 Many pt. have A-Fib & A-Flutter and move in & out between the two rhythms
 Both rhythmas arise from the same etiology (essentially the same dysrhythmia)
Management of A-Fib – New Onset
 Control the HR: first concern
o Ca Channel Blocker (diltiazem/cardizem) – IV, PO
o Beta-Blockers (metaprolol) – IV, PO
o Amiodarone (cordarone) – IV, PO  drug of choice to manage A-Fib
▪
▪

Ca Channel Blockers & Amiodarone are usually the first-line drugs depending on MD
Decreases conduction through the AV node & preventing chaotic impulses from
being transmitted to the ventricle
▪ Used if the pt. is post-surgical
Convert to Sinus Rhythm: second concern
o Electrical Cardioversion
o Pharmacologic methods (Abutalide – Corvert)
Electrical Cardioversion
 If the ventricular rate is above 150 & the pt. has serious signs & symptoms of being hemodynamically
unstable, prepare for immediate Cardioversion (may give a brief trial of medication)
o Serious S&S: SOB, hypotension, decreased LOC, chest pain, heart failure (S3&S4)
 Have O2 & IV in place; suction & intubation equipment should be available at the bedside
 Consider sedation (usually always Versed, Morphine, Diprivan)
 Synchronized Cardioversion:
o Narrow, regular………. 50-100J
o Narrow, irregular………120-200J (biphasic) or 200J (monophasic)
o Wide, regular…………. 100J
o Wide, irregular…………Defibrillation dose, unsynchronized
 Cardioversion should NOT be attempted if onset of A-Fib is >48 hours ago due to the high risk of
thromboembolism
 Pt. needs to receive anticoagulants before attempting to cardiovert them
 Sometimes perform a TEE to visualize whether or not there’s a clot in the RA – if not, will cardiovert
Pharmacologic Cardioversion
 Ibutilide (Corvert) – IV (need crash cart, ambu bag, emergency assistance – sends pt. into Asystole)
 Amiodarone (Cordarone) – IV, PO
o Not always used for the initial drug to convert
o Controls the HR during A-fib & can also prevent A-fib
 Flecainide (Tambocor) – PO
Persistent or Continuous A-Fib
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N418 – Exam 1
For the pt. who has persistent A-fib or did not convert after cardioversion…
Pt. will be on Beta-Blockers, Amiodarone, or Digoxin to control HR
o Amiodarone can cause thyroid issues
o Beta-blockers are not as effective as Amiodarone
o Digoxin is not the most current therapy to treat A-fib
 Anticoagulants (coumadin) to prevent thrombus formation
 Ablation/Maze procedure
o Cardiac cath to find the problem area, then destroy the tissue
o Pt. with new-onset tend to respond better to ablation than pt. with chronic A-fib
 New Drug: Dronederone (Multaq)  class III (substitute for Amiodarone – but NO thyroid issues)
Warfarin (Coumadin)
 Coumadin is one of the most widely prescribed anticoagulant medication in the world
 Indicated for prevention of thromboembolic events in pt. at risk
 Degree of anticoagulation varies widely among individuals & is affected by many drugs/foods
o Could have same type of person (height, weight, disease) – but it works differently






▪ INR values 2x week for first couple of weeks on Coumadin
▪ Afterwards, can monitor the INR once a month or once q2months
▪ Affects the clotting factors produced by the liver
o OA are particularly at risk for complications
o Rapidly absorbed by the GI tract
o Reaches maximum serum absorption in about 90 minutes
o Foods: green leafy vegetables, mayonnaise – limit these foods & be consistent with amounts
o Medications: Ibuprofen, Zantac
Antidote: Vitamin K (green leafy vegetables like spinach, broccoli, kale)
Takes 4-7 days to reach stable serum levels on fixed doses
Exerts anticoagulant effect through inhibition of clotting factors (primarily factor II – prothrombin)
Cost of Coumadin: 30 day supply is ONLY $4 – very inexpensive drug
International Normalized Ratio (INR)
 Following the INR closely, allowing a very narrow window of variability, results in fewer complications
 INR of 2-3 is recommended for most uses – exceptions include…
o Mechanical prosthetic heart valves: want INR of 2.5-3.5 (want better coagulation)
o Older adults, low protein, nutritional issues (want lower coagulation)
 Nursing Implications:
o Routine monitoring to ensure antithrombotic effect
 Interpreting INR:
o Pt. without anticoagulation should have INR at or near 1
o Levels lower than 2 are associated with increased incidence of thrombotic events
o Levels higher than 3 are associated with increased hemorrhage episodes
o If pt. is having surgery, they must be taken off of Coumadin before
Jantoven
 Another brand name for Warfarin/Coumadin
 Contraindications/Cautions:
o Pregnancy
o Active bleeding
o Spinal puncture
o Non-compliance
o Recent surgery (want INR <1.5 – especially if it was a very vascular area)
What’s New?
 Used for non-valvular atrial fibrillation (very expensive)
 No need to monitor INR
 Also used in the treatment of DVT/PE
 Dabitagran (Pradaxa):
72
N418 – Exam 1


o New PO thrombin inhibitor
o Used for non-valvular A-Fib
o Better at preventing strokes than Coumadin
o Effective within 2-3 hours of taking
o Advantages: no food or medication interactions; INR monitoring only once a year
o Disadvantages: expensive, taken BID & no antidote available in cases of overdose
Rivaroxban (Xarelto):
o Used for non-valvular A-Fib
o Also used for DVT prophylaxis for hip/knee surgery
o Antidote: PCC (prothrombin complex concentrate)
Apixaban (Eliquis):
o DVT prophylaxis for hip/knee surgery
Bridging
 Lovenox (LMWH) – fractionated heparin
o When pt. are currently taking Lovenox & are going to be moved to Coumadin, they must be
bridged
o Do not need to monitor PTT (only used for Heparin IV)
 30-40mg daily – DVT prophylaxis
 1mg/kg daily – weight based (FOR BRIDGING)
 When INR >or = 2.0…the Lovenox can be D/C & the Coumadin is continued
 Daily PT/INR
Additional Information
 Atrial Flutter responds better to ablation than A-Fib
 Coumadin is reversible through Vitamin K
o If a pt. has an INR level of 1.5 when their therapeutic window is 2-3, pt. will be placed on
Lovenox or Heparin to bridge the pt. until the INR is at the appropriate therapeutic level
 Heparin  monitor PTT
 Coumadin  monitor PT + INR
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N418 – Exam 1
(8) LRC/Skills – Chest Tubes, EKG/12-Lead Interpretation, Blood Administration, TPN & ACLS
Chest Tubes Overview
 Inserted to restore collapsed lung and/or to drain fluid from pleural cavity
 Tubing connected to sealed drainage system or one-way valve – this allows for:
o Removal of air & fluid from the chest cavity
o Keeps air from entering the chest cavity
o Prevents tension pneumothorax
 Water Seal: measures negative pressure in the chest cavity
o Inhalation  increase in negative pressure/rise in the chamber
o Exhalation  decrease in negative pressure/drop in the chamber
 Adding suction to system helps remove secretions
 Sterile disposable drainage systems: one-way valve or water seal; water- or dry-suction control
o Allows for the collection of smaller amounts of drainage
o Without suction, the nurse will read negative pressure level from calibrated chamber
▪ -10cm H2O negative pressure
o With suction, the nurse will add to reading from suction control & water seal chamber

▪ -20cm suction + -10 water seal = -30cm H20 negative pressure
For larger amounts of drainage or more accurate measurements – two chambers allows fluid to
drain into the collection chamber as air flows into the water-seal chamber
Types of Closed-Chest Drainage Systems
 Water-seal or One-way Valve:
o Water-seal chamber is the middle chamber (allows air to exit the pleural space on
exhalation & keeps air from entering on inspiration)
▪ Filled with sterile water up to the 2cm line
▪
Keep drain upright at all times & ensure fluid in water-seal chamber is at
recommended level
▪
o
Air-leak meter: higher the numbered column that has bubbling, the greater the air
leak
▪ Calibrated manometer: measures the amount of negative pressure in pleural cavity
(water level rises as the intrapleural pressure becomes more negative)
One-way valve replaces the traditional water seal
▪

Maintains seal even if unit is accidentally tipped over
▪ Monitor for air leaks (similar to water-seal device)
Wet- or Dry-Suction Control:
o Wet-suction control regulates amount of suction by the height of water in suction-control
chamber (left side)
▪ Fill suction-control chamber with sterile fluid to prescribed level (20cm)
▪
o
Connect suction source to suction-control chamber & then adjust amount of suction
to create gentle bubbling
Dry-suction control allows for higher suction pressure levels (quieter – no bubbling)
▪

Self-compensating regulator continuously balances force of suction with
atmosphere, which allows the system to respond & adjust to changes in air
leaks/fluctuations in suction source vacuum
▪ Set dial to -10 to -40cm H2O
▪ Adjust suction source until float ball appears in suction control indicator window
Mobile Chest Drains:
o Mobile chest drains are indicated for pt. who go home with closed-chest drainage still intact
or those who require early ambulation
o Heimlich valve: one-way flutter valve that allows air to escape but prevents it from reentering the chest cavity
▪ Accommodates small/partial pneumothoraxes (does NOT collect fluid)
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N418 – Exam 1
▪
▪
o
Arrow on housing of valve should always point AWAY from the pt.
Inner valve should not move during exhalation
Pneumostat: attaches directly to chest tube to collect fluid
▪
▪
▪
Useful for pt. with just a small amount of fluid drainage (looks like JP drain)
Bubbling in well after adding 1mL of water confirms air leak
Able to hold up to 30mL of fluid (emptied via Leur port)
Indications for Closed-Chest Drainage
 Used to treat pt. who have symptoms resulting from excessive accumulation of fluid or air in the
pleural cavity due to trauma, surgery, or disease
 Management of pleural or thoracic fluid after surgery achieved with closed-chest drainage
 Fluid:
o Due to trauma (hemothorax, chylothorax – leakage of lymph fluid from thoracic duct, or
disease processes such as CHF & cirrhosis)
o Empyema (high-protein exudative effusion resulting from infection in pleural space)
 Air:
o Causes loss of negative pressure (partial or complete pneumothorax)
o Can occur spontaneously, as complication of pre-existing pulmonary disorder, or as a result
of chest trauma
 Tension:
o Injury to chest wall or lungs allows air to enter space but stops air from escaping
▪ Considered a medical emergency
o
▪ Pressure becomes positive as air rapidly accumulates with each breath
Pneumothorax  leads to a mediastinum shift  causing a shift of thoracic organs to
unaffected side of chest (pressure on lung)  ventilation compromised  venous return to
heart impaired  hypotension, JVD, trachea displacement
Applying the Nursing Process
 Assessment:
o Vital signs
o Respiratory status (rate, depth, lung sounds, O2 saturation)
o Chest pain (PQRST)
o Difficulty breathing
o LOC
o Skin color/temperature
o Capillary refill
o Observation of insertion site (redness, swelling, excessive/unusual drainage; SQ emphysema)
o Functioning of drainage system – includes observing for:
▪ Amount of drainage, patency of tube, tidaling of fluid in water-seal chamber,
oscillations within air leak meter & suction-control chamber
 Planning:
o Enhancing gas exchange & tissue oxygenation are the primary goals

▪ Positioning, pain management, activity
o Place pt. in Fowler’s or high-Fowler’s position while in bed (facilitates lung expansion)
o TC&DB, ambulation, incentive spirometer, ADLs
o Preventing infection (dressing changes using surgical asepsis)
o Educate pt. to keep system below chest-level when sitting or ambulating
Implementation:
o HOB elevated 30 degrees or higher
o Position changes q2h
o Ambulation q4-6h during the day
o Pain medications
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N418 – Exam 1
o Change dressing regularly or PRN using sterile technique
Evaluation:
o Unlabored breathing, 12-20/min, O2 >90%, clear bilateral lung sounds, symmetric chest rise &
fall, no complaints of chest pain/dyspnea; warm & pink skin, capillary refill of <3 seconds
o Site free of infection, continuously functioning system, decrease in drainage over time
Maintaining Closed-Chest Drainage System
 Monitor pt. v/s & pain levels, auscultate breath sounds, observe pt. color & respiratory effort
 Check chest tube dressing q4h, palpate for crepitus or SQ emphysema
 Note the character, consistency & amount of drainage in collection chamber
 Coil tubing or lay horizontally across the chair/bed (avoids dislodgement)
 Maintain tubing below level of insertion
 Avoid dependent loops, kinks, pressure on tubing, lifting drainage system above pt. chest
 Clotting in tubing – nurse should check with MD about milking the tube
 Encourage pt. to cough frequently & to do breathing exercises, incentive spirometery, ambulation
 Always keep (2) rubber-tipped clamps at bedside to clamp
 Notify MD immediately of any of the following:
o Cyanosis, rapid or shallow breathing, SQ emphysema, chest pain, excessive bubbling, or a
temperature > 101 degrees
 Continuous observation for tidaling
 Removal of chest tube is only done if chest x-ray shows that the lung has re-expanded

Managing Complications
 Patency:
o Look for loose connections
o Determine if clamped, kinked, or occluded
o If tubing is disconnected, instruct pt. to exhale & cough  clamp the tube  submerge end
of tube in 1 inch of sterile water  reconnect quickly
o Tighten loose connections & tape securely
 Air Leak:
o Indicated by excessive or continuous bubbling in water-seal chamber or air-leak meter
o Use clamps to locate the leak by clamping at various points along tube beginning at the
proximal end near dressing (if it stops, the leak is at insertion site or inside chest)


▪ Examine site to see if dressing is loose or tube is dislodged
▪ Ask pt. to cough, apply occlusive dressing & monitor for oxygenation status
o Hissing, large amount of new drainage, or visibility of drainage holes at the proximal end of
the tube indicates that the tube as dislodged – notify MD immediately
If a chest tube disconnects from a closed-chest drainage system, quickly clamp the tube as long as
there is no bubbling in the water-seal/air-leak meter.
If a chest tube is completely dislodged, cover the site immediately with a sterile gauze dressing – if
you can hear air leaking out of the site, make sure the dressing is not occlusive.
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N418 – Exam 1
EKG Interpretation
 Sinus (SA) node  60-100 bpm
 Atrial (AV) node  40-60 bpm
 Purkinje fibers  20-40 bpm
 EKG Paper: small box (0.04secs); large box (0.20secs/5 small boxes); 30 large boxes (6secs)
Segments & Intervals
 P wave:
o Atrial contraction
o Normal Duration: <0.10 seconds
o Longer & taller P waves result from LA enlargement (pulmonary HTN, COPD, ASD)
 PR interval:
o First inflection of P wave to beginning of QRS complex
o Represents the conduction of impulses from SA node to the ventricle
o Normal Duration: 0.12-0.20 seconds
o Long PR interval typically indicates first degree AV block
 QRS complex:
o Ventricular contraction – first negative inflection of Q to the end of S wave
o QRS helps determine whether dysrhythmia is ventricular or supraventricular
o Normal Duration: <0.12 seconds or 0.04-0.10 seconds
o You will not always see all three waves
 QT interval:
o Beginning of Q to the end of T
o Normal Duration: 0.32-0.44 seconds (needs to be corrected for HR)
 ST segment:
o Usually isoelectric meaning that it should remain at baseline
o Decreased: typically indicates ischemia – >0.5mm change in 2 or more contiguous leads
o Increased: typically indicates infarction – >1mm change in limb leads & >2mm change in 2
or more precordial leads (tombstone appearance)
 T wave:
o Ventricular repolarization (relaxation)
o T wave inversion typically indicates ischemia
o Tall, peaked T waves associated with hyperkalemia (inc. K)
o Hyperacute T waves commonly occur with MI
 Q wave:
o >0.04 & deeper than 25% of the height of R wave  abnormal & indicates infarction
o Q wave represents infarcted tissue (death of tissue)
Rhythm Interpretation Checklist
1. Rhythm Check
-Is it regular?
-Is it irregular?
-Are there any patterns to the irregularity?
2. Rate
-What is the exact rate?
-Is the atrial rate the same as the ventricular rate?
a. 6-Second Method: count QRS complexes in 6-sec strip & multiply by 10
b. Large Box Method: count # of large boxes between two consecutive waveforms & divide
into 300
c. Small Box Method: # of small boxes between two consecutive waveforms & divide into 1500
3. P Waves
-Are P waves regular, upright and slightly rounded? Do they all look similar?
-Is there one P wave for every QRS
-Do they all the P waves look alike?
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N418 – Exam 1
-Are the irregular P waves associated with ectopic beats?
4. PR Interval
-Is the PR interval measurement normal?  0.12-0.20 seconds
-Are the PR intervals constant?
-If the PR interval varies, is there a pattern to the changing measurements?
5. QRS Complex
-Is the QRS complex measurement normal?
-Do the QRS complexes look similar (of equal duration)?
Sinus Rhythms
 Normal Sinus Rhythm:
o Rhythm is regular with constant R-R intervals & constant P-P intervals
o Rate of 60-100 bpm
o P wave occurs before each QRS complex
 Sinus Bradycardia:
o Rate of <60 bpm
 Sinus Tachycardia:
o Rate of >100 bpm BUT <180 bpm
 Sinus Arrhythmia:
o Rhythm is irregular
o P wave occurs before QRS complex & all P waves look alike
Atrial Arrhythmias
 Premature atrial complexes (PAC):
o Rhythm irregular due to premature beats
o Rate is usually normal
o P wave: occurs prematurely; may differ in shape from sinus P wave
o QRS complex is normal with a duration of 0.04-0.10 seconds
 Atrial flutter: (sawtooth appearance)
o Rhythm often regular but depends on conduction through AV node (can be irregular)
o P wave: called “flutter waves”; creates an atrial rate of 250-450 bpm
o PR interval is not measureable
o QRS complex is normal
 Atrial fibrillation:
o Rhythm is irregularly irregular
o P wave: atrial rate of 400-600 bpm
o PR interval is not measureable
o QRS complex is normal
Ventricular Dysrhythmias
 Premature Ventricular Complexes (PVC):
o Rhythm regular except for ectopic beat
o Rate of 60-100 bpm
o P wave before each QRS complex except ectopic beat with wide complex
o P waves look alike with a normal PR interval of 0.12-0.20 seconds
o QRS complex widened on ectopic beat
 Ventricular Tachycardia (V-Tach):
o Rhythm regular
o Rate >100 bpm
o P wave is usually absent
o No PR interval is present
o QRS complex wide & bizarre, but uniform (>0.12 seconds)
 Ventricular Fibrillation (V-Fib):
o Rhythm irregular, rapid & chaotic
o Rate cannot be determined
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N418 – Exam 1
o P wave, PR interval, nor QRS complex is discernible
AV Blocks
 First Degree AV Block:
o Not a true block
o Delay at AV node
o Each impulse is eventually conducted
o Prolonged PR interval (>0.20 seconds)
 Second Degree AV Block:
o Type I (Wenchebach, Mobitz I) –
o

▪ Intermittent block – some beats are conducted, but others are blocked
▪ Prolonged PR interval until P wave occurs with NO QRS complex then cycle restarts
▪ Pathology occurs at level of the AV node
Type II (Mobitz II) –
▪ Intermittent block – some beats are conducted, but others are blocked
▪ PR intervals are constant (normal or slightly prolonged)
▪ Pathology occurs at the Bundle of His or bundle branches
Third Degree/Complete Heart Block:
o Atrial & ventricles are completely dissociated
o Complete block occurs at the AV node
o Ventricular rate <40 bpm
12-Lead EKG Interpretation
 12 Lead EKG: (#1 priority with pt. presenting with chest pain)
o Central to initial risk & treatment stratification – elevated enzymes are NOT necessary for a
decision to administer fibrinolytics or perform PCI (pt. presenting with ST elevation requires no
other clinical evidence to be sent to the cath. lab)
o Principle: ischemic/necrotic tissue does not conduct electrical
impulses normally – reperfusion dysrhythmias
 Localization of Infarction:
o Septal  V1, V2
o Anterior  V3, V4
o Lateral  I, aVL, V5, V6
o Inferior  II, III, aVF
 Coronary Circulation:
o Right Coronary Artery
▪ RA  RV  SA Node  AV bundle  Posterior LV 
Inferior
▪ If pt. has occlusion of the right coronary artery – we
would see loss of P-wave, bradycardia due to disruption of main SA node conduction
o Left Coronary Artery
▪ Left anterior descending
 Anterior 2/3 of inter-ventricular
septum
 Anterior LV
 Lateral LV
 Supplies most of the left side of the
heart
▪ Circumflex (circles around)
 LA
 Posterior LV
 Lateral LV
▪ Much better to have right-sided MI than
left
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N418 – Exam 1
▪

Blockage in the left main artery commonly called the “widow maker”
Relationship between LV Surface, EKG Lead & Coronary Artery:
ECG Leads
Artery Involved
Inferior
II, III, aVf
RCA (80-90%)
LCX (10-20%)
Infero-lateral
II, III, aVf, V5, V6
LCX
Lateral
V5,2 V6, I, aVL
LCX
Anterior
V2, V3, V4
LAD, LM
Septal
V1, V2
LAD
Antero-septal
V1, V2, V3
LAD
Posterior
V1, V2 (reciprocal)
LC or RCA

-SALLI METHOD-
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N418 – Exam 1
Blood Administration
 How to handle blood safely:
o Use 18-20 gauge or larger IV catheter
o Use closest Y-port on primary tubing to reduce the risk of precipitation or hemolysis in the
primary tubing
o Use appropriate tubing for blood administration
o Only hang with NS – never add/infuse meds & IV solutions unless they have met two criteria:
▪
▪



Must be FDA-approved for use with blood products
Documentation must be available to show that the addition is safe & does not
adversely affect the blood component
o Never use dextrose-containing solutions with blood (glucose causes RBC aggregation)
o Administer the blood products no faster than 2mL/hr
Preventing contamination of blood products:
o Hang blood products within 30 minutes of receiving blood
o Transfuse the products within 4 hours
Blood product & pt. identification:
o Consent must be obtained from pt. to receive blood
o First obtain proper identification of pt. to obtain type & cross-match from
o Compare the pt. info to the request for blood form with another nurse
o Draw type & cross-match, label the tube appropriately with designated label
o Retrieve blood from the lab – two HCP must match pt. identifiers (name, medical record
number, unique band number) & blood (type, unit number, unique identifier, compatibility &
expiration date) with the blood & request form
o All of the above must be performed again with two nurses at the pt. bedside
Blood product transfusion:
o Blood must be hung within 30 minutes after receiving from the lab
o Obtain vital signs before administering
o Hang as a piggy back with NS only
o Must be hung with appropriate tubing
o Monitor for 15min after starting transfusion & obtain vital signs –
▪ If reaction occurs (SOB, rash, fever, etc.), the nurse should stop the transfusion,
perform an assessment, notify the MD, notify the blood bank, obtain a blood & urine
sample, document & advise your pt. to notify future providers about this reaction
o Transfusion must be completed within 4 hours
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N418 – Exam 1
Advanced Cardiac Life Support: ACLS Overview
Treatable Causes
 H’s:
o Hypoxia
o Hypothermia
o Hypovolemia (bleeding, vomiting, diarrhea, high fever/sweating)
o Hydrogen ion (acidosis – diabetics, respiratory, renal failure)
o Hypo-/Hyperkalemia
 T’s:
o Toxins (cocaine, psychiatric medications, etc.)
o Tamponade (collection of blood within the pericardial sac)
o Tension pneumothorax
o Thrombosis (coronary or pulmonary)
ACLS Skills
 Advanced Airway:
o Endotracheal Tube (ET)
o Laryngeal Mask Airway (usually used for small, quick procedures)
o Combitube (blind intubation when you cannot visualize the vocal cords)
 Medications:
o Nurses needs to be knowledgeable of medications, dosages, times, SE
 Electrical Therapy:
o Transcutaneous Pacing (TCP): typically used for pt. with bradycardia
o Direct Countershock
o Cardioversion (direct current defibrillation)
o Defibrillation (used only for v-tach & v-fib)
Defibrillation vs. Cardioversion
 Defibrillation:
o Pulseless V-Tach or V-Fib
o Unsynchronized
o Paddles (handheld gel pads – 25 lbs. pressure; also have hands-free)
o Energy Levels (200J for biphasic; 360J for monophasic)
 Cardioversion:
o Tachycardia with a pulse
o Synchronized with the “R” wave
o Energy Levels –
▪ Narrow Regular  50-100J
▪
▪
▪
Narrow Irregular 120-200J for biphasic; 200J for monophasic
Wide Regular  100J
Wide Irregular  administer defibrillation doses – NOT synchronized
Synchronized Electrical Cardioversion - Procedures
 Oxygen, IV, Cardiac monitoring, Defibrillator at pt. bedside
 Connect defibrillator to the EKG leads & monitor in Lead II
 Sedation may be used (Valium, Versed, Diprovan) – cardioverted pt. usually awake, alert, talking
 Turn on the “SYNC” button on the defibrillator
 Observe marking of QRS complexes
 Charge to desired energy setting  press & hold shock (shock occurs when with QRS complex)
 If pt. rhythm is V-Fib or Pulseless V-Tach, be sure to “un-synchronize” before shocking
Waveform Capnography
 Normal ETCO2 in the adult pt. should be 35-45mmHg
 Measures the quality of chest compressions (high-quality compressions are 10-20mmHg)
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N418 – Exam 1

Indicator of return of spontaneous circulation
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N418 – Exam 1
Adult Cardiac Arrest
 Important to have 2 established IV lines (preferably 18 gauge – bigger the better)
 Oxygen @ 100% FiO2 – all the way up to 15L & connect Ambubag
 Epinephrine is the first drug of choice (1mg q3-5min)
 Amiodarone is the second-line drug (300mg bolus for arrest followed by 150mg bolus)
 Vasopressin (40units usually only given the first or second dose; only given q10min)
o Epi & Vasopressin are to jumpstart the electrical conduction system
o Amiodarone is used for controlling dysrhythmias once electrical activity is started
 Goal: whatever converts a pt. to a perfusable rhythm usually the IV drip that is started
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N418 – Exam 1
Bradycardia Algorithm
 Only treated when the rhythm produces symptoms
 Drugs that can induce bradycardia: Ca Channel Blockers, Beta-Blockers, Digoxin
 Treatment:
o Atropine: maximum dose of 3mg – only allowed to provide 6 doses
o Dopamine: can be used for BP (may also speed up HR)
o Epinephrine: typically used for intense BP support
85
N418 – Exam 1
Tachycardia Algorithm
 Requires treatment when rhythm starts producing hemodynamic instability
 Adenosine: slows the HR down enough to visualize the QRS complex & Dx (very short-acting – will
usually see drop in pt. HR within seconds)
 Vagal Maneuvers: increases intrathoracic pressure & slows HR down (coughing or bearing down)
 Sotalol: belongs to class of Beta-Blockers (also called Beta-Pace)
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N418 – Exam 1
Post-Cardiac Arrest Care
 Maintain oxygenation >92%
 Assess both the SBP & MAP
 Rule of Thumb: circulating volume is necessary for the use of Vasopressin – always give volume first
o Fluid of choice is NS (isotonic)
 Asses pt. neurological status
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N418 – Exam 1
Pre-Hospital Fibrinolytic Checklist
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N418 – Exam 1
Management Goals: Patient with Suspect Stroke
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N418 – Exam 1
Acute Coronary Syndromes Algorithm
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N418 – Exam 1
TPN – Total Parenteral Nutrition
 Parenteral nutrition refers to the administration of nutrients by a route other than the GI tract
 Indications for Parenteral Nutrition:
o Chronic severe diarrhea & vomiting
o Complicated surgery or trauma
o GI obstruction, severe anorexia nervosa
o Severe malabsorption, short bowel syndrome, GI tract anomalies & fistulas
 Composition of Parenteral Nutrition:
o Base solutions contain dextrose & protein in the form of amino acids
▪ Pharmacy then adds the prescribed electrolytes, vitamins & trace elements
A three-in-one or total nutrient mixture containing an IV fat emulsion, dextrose & amino acids
is widely use
Calories of Parenteral Nutrition:
o Calories in PN are supplied primarily by carbohydrates in the form of dextrose & by fat in the
form of fat emulsions (recommended energy intake of 25-35cal/kg/day)
o Fat emulsions provide approximately 1cal/mL (10% solution) or 2cal/mL (20% solution) – these
emulsions contain soybean, safflower triglycerides with egg phospholipids
▪ IV fat emulsions provide up to 30% of total calories
▪ Important to monitor triglyceride levels
▪ Should be given over a course of 8-10 hours with a rate no faster than 0.11g/kg/hr
o



▪ N/V & elevated temperature has been reported when lipids are infused too quickly
▪ Contraindicated: pt. with disturbance in fat metabolism such as hyperlipidemia
Methods of Administration:
o Pt. receiving parenteral nutrition must be able to tolerate a large volume of fluid
o Central Parenteral Nutrition (TPN) –
▪ TPN is indicated when long-term support is necessary or when pt. has high protein &
caloric requirements
▪ May be given through a central venous catheter or PICC line through a large central
vein so that rapid dilution can occur
▪ TPN is hypertonic with high glucose content ranging from 20%-50%
o Peripheral Parenteral Nutrition (PPN) –
▪ PPN is indicated when:
 (1) Nutritional support is needed for only a short time, (2) protein & caloric
requirements are not high, (3) risk of a central catheter is too great, or (4) the
PN is being used to supplement inadequate oral intake
▪ Administered through a peripherally inserted catheter or vascular access device,
which uses a large vein
Complications of Parenteral Nutrition:
o Refeeding Syndrome –identified by fluid retention & electrolyte imbalances (low P, K & Mg)
▪
o
o
o
Predisposition to refeeding syndrome present in pt. with long-standing malnutrition
states, such as alcoholism, N/V/D, chemotherapy & major surgery
▪ Hypophosphatemia is the hallmark of refeeding syndrome (associated with
dysrhythmias, respiratory arrest & neurologic disturbances – paresthesia)
Infection
Metabolic problems (hyper/hypoglycemia, altered renal function, hyperlipidemia)
Catheter-related problems (air embolus, pneumothorax, hemorrhage, dislodgement,
phlebitis, thrombosis of vein)
Parenteral Nutrition Crossword
 Infusing TPN through a peripheral IV could possibly result in thrombophlebitis
 Regular IV solutions such as 5% dextrose or D5LR do not contain protein
 Close monitoring of triglyceride levels is required for critically ill pt. receiving fat emulsions
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N418 – Exam 1



Potential side effect of infusing lipids too quickly – vomiting
Provides a large number of calories in a relatively small amount of fluid – lipids
Pt. undergoing stress increases the need for protein intake to 1.5-2g/kg/day
92