NCM 118Lecture:LIFE

THREATENING

MICHAEL JEB TORIENTE RN,|MAN

WEEK4 and 5

TABLE OF CONTENTS
I. Pain (Synchronous VII. Death and Dying
Lecture Notes
09/03/2021) (Additional Reading;
PPT)
II. Shock (Osmosis
Supplemental Video) VIII. Life-Span
Development
III.Introduction to Twelfth Edition: Death,
Shock Dying and Grieving
(Recorded Lecture) (Additional
Reading; PPT)
IV. Types of Shock
(Recorded Lecture) IX. Shock (Synchronous
Lecture 09/03/2021)
V. SIRS – SEPSIS – Pain is defined differently which is why you treat
SEVERE X. Synchronous Lecture pain differently from one person to another
SEPSIS (Recorded (09/04/2021)
•
Lecture) Cycle by which pain happens
•
VI. Dying and Inadequate Pain Assessment and Treatment o Your
Death management for pain is defined on how you assess
(Recorded Lecture) it

PAIN (SYNCHRONOUS LECTURE 09/03/2021) o For pediatrics: Wong-Baker Scale o

PAIN Inadequate pain assessment will lead to
inadequacy in pain treatment
•
PADIS (Pain, Agitation/Sedation, Delirium, Immobility,
and Sleep Disruption in Adult Patients in the ICU) Common Painful Procedures in the ICU
Guidelines gives recommendations •
for pharmacological and Arterial line insertion

nonpharmacological ways of treating pain o •

Peripheral IV insertion
Clinical practice guidelines wherein there are alot of
•
recommendations that are clinical based evidence Central line insertion • Peripheral blood draw
•
PICO and Descriptive Question for PADIS Clinical Femoral sheet removal
Practice •
Respiratory exercises
Guidelines
•
Mouth care
•
Eye care
•
Turning/Mobilization
•
Nasogastric tube insertion
•
Nursing Care (ex. repositioning)
•
Extubation

Question: What factors influence pain in critically

ill adults during both rest and during
procedures? Ungraded Statements:
Wheel of PAIN Misfortune •
Pain at rest is influenced by both psychological
(e.g., anxiety, depression) and demographic (e.g.,
young age, one or more comorbidities, past history
of surgery) factors.

NCM 118 LEC

 • •
Pain during a procedure is influenced by Analgesia-first Sedation o An analgesic (usually
preprocedural pain intensity, the type of procedure, an opioid) is used before a sedative to reach the
underlying surgical trauma diagnosis and sedative goal
demographic factors (younger age, female sex, and
non-white ethnicitiy) o To help in alleviating the o Uses sedative later on
pain of the client for a certain procedure, explain to •
the client the procedure, the process, what to Analgesia-Based Sedation o An analgesic
expect, etc. (usually an opioid) is used instead of a sedative to
reach the sedative goal
Question: What are the most reliable and
valid pain assessment methods to use in o No sedatives at all the management will
critically-ill adults? Ungraded statements: depend on just giving the patient an
analgesia
•
Self-report scales o A patients’ self-report of pain
is the reference standard for pain assessment in Key Concepts with Analgosedation
patients who can communicate reliably •
Takes advantage of certain opioid properties o
o Among critically ill adults who are able to Reduces/eliminates sedative requirements and
self-report pain, the 0-10 NRS their associated ADRs
administered either verbally or visually is
a valid and feasible pain scale. o Improves sedation-agitation scores o
Dyspnea & respiratory depressant
•
Behavioral assessment tools o Among critically •
properties May accentuate opioid-
ill adults unable to selfreport pain and in whom
behaviors are observable, the Behavioral Pain Scale related ADR’s o Gastric dysmotility,
in intubated (BPS) and non-intubated (BPS-NI) delirium, hypotension, myoclonus, chest
patients and the Critical Care Pain Observation Tool wall rigidity
(CPOT) demonstrate the greatest validity and
reliability for monitoring pain
•
May not be appropriate for patients with GABA
• agonist/sedative needs:
Proxy reporters o When appropriate, and when
the patient is unable to self-report, family can be o alcohol/drug withdrawal & drug
involved in their loved one’s pain assessment intoxication o Neuromuscular blockade o
process
Elevated intracranial pressure & status
▪ Ensure that the patient who will epilepticus
talk on behalf of the patient has a
direct contact with the patient Multimodal Analgesia
(family member who takes care •
of the patient, private nurse, Definition o Combining different analgesics that act
caregiver, etc) by different mechanisms and at different sites in
the nervous system, resulting in additive or
•
Physiologic measures o Vital signs (ex. Heart synergistic analgesia with lowered adverse effects
rate, blood pressure, respiratory rate, oxygen compared to sole administration of individual
saturation, end-tidal CO2) are not valid indicators analgesics
for pain in critically ill adults and should only be •
used as cues to initiate further assessment using Also known as “balanced analgesia”
appropriate and validated methods such as the •
patient’s self-report of pain (whenever possible) or Established in 1993
a behavioral scale (ex. BPS, BPSNI, CPOT) •
Recommended by perioperative practice guidelines
Protocol-Based Pain Limited ICU literature
Assessment/Management
Multimodal Analgesia
PICO Question
PICO Question
P Critically ill adult patients in an ICU
I Protocol based (analgesia/analgosedation) pain P Critically ill adult patients in an ICU
assessment and management program
I Adjunctive
C Usual Care •
O Pain intensity Acetaminophen (IV/PO/PR)
Medication exposure (opioids and sedatives) •
Adverse Events Ketamine
Duration of Mechanical Ventilation •
Neuropathic analgesia
ICU Length of Stay
•
IV Lidocaine
Analgesia-First versus Analgesia-Based Sedation

•
 • Adjunctive Neuropathic Pain Medication
NSAID (IV/PO)
Recommendations:
C No use of the adjunctive intervention
• We recommend using a neuropathic pain
O • medication (ex. Gabapentin, carbamazepine, and
VAS score at 24 hours postoperatively (in
pregabalin) with opioids for neuropathic pain
cm)
management in critically ill adults (strong
• recommendation, moderate quality of evidence)
Mean BPS pain scores until patient is
extubated • We suggest using a neuropathic pain medication
(ex. Gabapentin, carbamazepine, and pregabalin)
• with opioids for pain management in ICU adults
Pain score at extubation
after cardiovascular surgery (conditional
• recommendation, low quality of evidence)
Time to extubation (minutes)
• Multimodal Analgesia
Rescue opioid doses
• Evidence Gaps:
Opioid consumption (in morphine
• Each adjective non-opioid analgesic requires larger
equivalents) studies on critically ill adults to clearly evaluate
their opioid-sparing properties and their ability to
Adjunctive Acetaminophen (IV/PO/PR) reduce opioid-associated adverse effects
Recommendation: • Little data on medical ICU patients
• • Safety concerns related to specific non-opioid
We suggest using acetaminophen as an adjunct to
analgesics need to be evaluated in critically ill
an opioid to decrease pain intensity and opioid
consumption for pain management in critically ill
•
adults Optimal dose and route of administration
adults (conditional recommendation, very low
unclear
quality of evidence)
• Efficacy and safety data of combination non-opioid
analgesic required
Adjunctive Low-Dose Ketamine
Recommendation: Pharmacological Interventions to Reduce
We suggest using low-dose ketamine (0.5mg/kp IVP x 1; 1-2 Procedural Pain
mcg/kg/min) as an adjunct to opioid therapy when seeking PICO Question
to reduce opioid consumption in post-surgical adults
admitted to the ICU (conditional recommendation, very low P Critically ill adult patients in an ICU
I • Opioid (vs. no opioid)
quality of evidence)
• High dose (vs. low-dose opioid)
IV Lidocaine • Local analgesia
No difference in the one available ICU RCT for:
• Nitrous oxide
• Self-reported pain
• Volatile anesthetics
• Opioid equivalence
• NSAIDs
• ICU LOS
C No use of the analgesic intervention
• Hospital LOS
O • Pain (intensity) score
Recommendation: • Opioid exposure/use
• We suggest not routinely using IV lidocaine as an • Adverse events
adjunct to opioid therapy for pain management in • Patient satisfaction with pain relief
critically ill adults (Conditional recommendation,
low quality of evidence)
Note: Many procedural pain RCTs use Chest Tube Removal
(CTR) as the paradigm ICU pain procedure (is painful and
Adjunctive NSAIDs easy to standardize) but the degree to which data from CTR
• 2 small RCT in ICU o Cardiac surgery o Abdominal studies can be extrapolated to other painful ICU procedures
surgery remain unclear

• No difference in pain scores at 24 hours

Procedural Treatment - Opioid vs. No Opioid
• Small reduction in opioid consumption
• No difference in ADRs

Recommendation:
• We suggest not routinely using a COX-1 selective
Recommendation:
NSAID as an adjunct to opioid therapy for pain
management in critically ill adults (Conditional • We suggest using an opioid, at the lowest effective
recommendation, low quality of evidence) dose, for procedural pain management in critically
ill adults (conditional recommendation, moderate
level

NCM 118 LEC

 of evidence) intravenously, orally or rectally as an alternative
to opioids for pain management during discrete
Remarks:
and infrequent procedures in critically ill adults
• The same opioids (ex. Fentanyl, hydromorphone, (conditional recommendation, low quality of
morphine, and remifentanil) that are recommended evidence)
in the 2013 PAD guidelines to manage pain should
also be considered when an opioid is deemed to be
•
We suggest not using an NSAID topical gel for
the most appropriate pharmacological intervention procedural pain management in critically ill adults
to reduce procedural pain. (conditional recommendation, low quality of
evidence)
• Important to time the administration of opioid so
that peak effect coincides with the procedure
Non-Pharmacological Interventions to Reduce
Pain
IV Lidocaine
PICO Question

P Critically ill adult patients in an ICU

I • Cybertherapy
• Hypnosis
Considerations: • Massage
No evidence lidocaine is beneficial
• • Music
One RCT tested SQ infiltration of 10mL of 0.5% • Cold therapy
bupivacaine (around CTR site) vs. 50% nitrous
oxide showed decreased pain scores with
• Relaxation techniques

• C No use of the analgesic intervention

bupivacaine High risk of bias RCT; bupivacaine O • Pain (intensity) score
only administered by anesthesiology personnel
• Opioid exposure/use
•
nitrous oxide has not been evaluated for procedural • Adverse events
pain in the ICU Recommendation: • Patient satisfaction with pain relief
•
We suggest not using either local analgesia or
Cybertherapy (Virtual Reality) or Hypnosis
nitrous oxide for pain management during chest
tube Considerations
removal in critically ill adults (conditional •
recommendation, low quality of evidence) Only one RCT evaluated cybertherapy and
hypnosis, respectively
Volatile Anesthetics (ex. Isoflurane) •
Each RCT had a high risk of bias and the
Considerations:
intervention minimally reduced pain.
•
No RCT comparing volatile anesthetic to opioid for •
procedural pain Important feasibility consideration for each
intervention
•
Increased resources and potential safety concerns
with administering gases in the ICU
•
Recommendation:
We recommend not using inhaled volatile
anesthetics for procedural pain management in
critically ill adults (strong recommendation, very
low quality of evidence)

NSAIDs
Considerations:
•
One RCT found that pain scores similar after CTR
between morphine 4mg IV x 1 vs ketorolac 30mg IV
x
1
•
One RCT found topic valdecoxib gel vs. placebo
reduced post CTR pain scales but no data vs. other
analgesics
Recommendation:
•
We suggest using an NSAID administered

•
Recommendation: •
Although a pooled analysis of studies demonstrated
•
We suggest not offering cybertherapy (virtual a non-significant reduction in pain intensity (0-10
reality) or hypnosis for pain management in NRS) with cold therapy (MD -1.91 cm; 95% CI [-5.34
critically ill adults (conditional recommendation, to +1.52]; low quality), the panel considered that a
very low quality of evidence) reduction of this magnitude on the NRS scale was
clinically important and consistent with meaningful
acute pain reductions (1.3 to 2.4 cm) as defined in
Massage Therapy
one study of 700 post surgical patients.

Recommendations:
•
We suggest offering cold therapy for procedural
pain management in critically ill adults (conditional
• •
Considerations: Five RCT;s in cardiac or abdominal recommendation, low quality of evidence)
• Remarks: Cold ice packs were applied for 10
surgery patients in the ICU Pooled analysis showed
reduction in pain intensity: minutes, and wrapped in dressing gauze, on the
area around the chest tube before its removal
o MD = -0.8cm, 95% CI [-1.18 to -0.42]; low
quality Relaxation Therapy
•
No adverse events reported
•
Feasibility influenced by duration of intervention
and who administers it Recommendation:
•
We suggest offering massage for pain management Recommendation:
in critically ill adults (conditional recommendation, •
low quality of evidence) We suggest offering relaxation techniques for
procedural pain management in critically ill adults
(conditional recommendation, very low quality of
Music Therapy
•
evidence) Remarks: the relaxation technique
used in each study differed

SHOCK (Osmosis Supplemental Video)

Ischemia
•
VAS Pain Score Lack of blood flow to a specific area of tissue
•
For example in a heart attack, the coronary artery
of the heart gets blocked that supplies the left
ventricle with blood. That localized area of heart
Considerations: tissue does not get enough blood and oxygen. This
• damage is localized to the left ventricle.
Pooled analysis of n=5 RCTs demonstrated that

music reduced 0-10 VAS pain intensity o MD -

0.52cm; 95% CI (-1.49 to +0.45); low quality

•
Less benefit seen for patients with procedural pain
(n=2 RCTs) vs. non-procedural pain (n=3 RCTs -
•
post cardiac surgery) Patients’ preference for
•
music is an important consideration Feasibility
concerns for some interventions (ex. Music
performer in ICU) Recommendation:
•
We suggest offering music therapy to relieve both
non-procedural and procedural pain in critically ill
adults (conditional recommendation, low quality of
evidence)

Cold Therapy
Considerations:
•
Cold therapy prior to CTR evaluated in 2 RCTs

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

Shock that stroke volume goes
• down as well, which
It is similar to Ischemia but on a global scale. causes cardiac output to
• go down, and blood
It is a whole body circulatory failure. pressure goes down as
• well.
The blood flow to the tissues is dangerously low,
leading to cellular injury; possibly damaging • When the cardiac output
multiple organs or even lead to multiple organ goes down,
catecholamines like
failure if not treated immediately.
epinephrine and
• norepinephrine, ADH
With shock, tissues of the body do not get enough and Angiotensin II are
oxygen in the blood. Normally, blood perfuses released. All of which
through tissue and delivers oxygen because there cause vasoconstriction
is enough pressure in the circulatory system to of the blood vessels
push it through. Blood pressure is a major which increases vascular
determinant for the amount of blood perfusing resistance and increases
• heart rate which
through tissues. Blood pressure is increases cardiac
determined by two components: the resistance to output.
blood flow in the blood vessels (such as vessel ▪ Non-hemorrhagic Shock
length, blood viscosity, and vessel diameter)
and the cardiac output (the volume of blood
• The loss of the fluid
pumped by the heart through the body per volume is not because of

minute). o Cardiac Output can be divided into bleeding. • An

example would be
two: Heart Rate (beats/min) time Stroke
severe dehydration. Loss
Volume (blood pumped/beat) ▪ The of fluid in sweat would
Stroke Volume is found by taking the reduce blood volume to
total volume of blood leftover after where it wouldn't be enough
contraction (End Systolic Volume) and to supply the body’s organs
subtracting it to the total volume of and you develop
the heart after filling (End Diastolic hypovolemic shock.
Volume)

o The super important indicator of tissues not getting

enough oxygen due to hypovolemia is a decreased mixed
venous oxygen saturation or (MVO2). o MVO2 is the
3 Categories of Shock and their Subcategories
amount of oxygen bound to hemoglobin in blood coming to
• Hypovolemic Shock o Shock induced by the right side of the heart from the tissues. So it’s like the
a low fluid volume of blood amount of oxygen leftover or not extracted and used by the
o Can be categorized as non-hemorrhagic and tissues. o If blood volume is down, oxygen is down, and
hemorrhagic shock. there is going to be less leftover. So, MVO2 will be down
with hypovolemic shock. o Since blood flow provides heat
▪ Hemorrhagic Shock to the tissues, when it’s down, the skin starts to feel cool
• Loss of blood volume and clammy. And so, hypovolemic shock is considered a
through rupture blood “cold shock”. • Cardiogenic Shock o Cardiogenic =
vessels. produced by the heart o This is when something happens
• Caused by bleeding • A to the heart (ex. trauma) such that now it cannot pump
loss of about 20% of enough blood to the body’s tissues. The most common
your total blood volume cause is Acute Myocardial Infarction (MI) or Heart Attack. o
(roughly 1L) could be The heart attack itself reflects ischemia, but the effects of
enough to induce the initial cardiac damage, eventually leads to a state of
hypovolemic shock. • shock. o When the heart’s muscle cells die, it
When this liter of blood produces weaker contractions which means
leaves the circulation, the amount of blood pumped out or stroke volume
the total filling volume goes down and therefore cardiac output goes down
of the heart goes down as well. o In the same way as with hypovolemic
(end diastolic volume
shock, the body releases vasoconstrictors to
goes down). This means

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 increase vascular resistance and help maintain often depleted or used up during
blood pressure. o Also as with hypovolemic shock, sepsis leads to this net increase
MVO2 will be down, there is less oxygen being in coagulation and clotting in the
microvasculature. Clotting and
pumped out and so less will be left over. o blockages in the blood vessel
Sometimes there might be an obstruction that does further decreased perfusion.
not allow the heart to fill properly with blood. For
example, we might have the pericardial sac fill up ▪ This widespread vasodilation
with fluid due to an infection, or blood from a means very little vascular
traumatic accident like getting stabbed in the resistance and blood cannot get
chest. If this sac fills up, it physically constricts the the chance to unload as much
heart from expanding and contracting normally and oxygen as it cruises through the
also reduces the stroke volume. This is sometimes vasculature. And it gets back to
the right side of the heart with
sub classified as obstructive shock. o Similarly
leftover oxygen. In this case, as
to hypovolemic shock, a reduction in cardiac output opposed to cardiogenic and
leads to lower blood flow so the skin gets cool and hypovolemic shock, MVO2 can be
clammy and so cardiogenic shock is also normal or even increased.
considered a kind of cold shock.
▪ In contrast to hypovolemic and
• Distributive Shock cardiogenic shock, now there is
o There is typically a leakiness of the blood an increase in blood flow in the
vessels and an excessive amount of arterial peripheral blood vessels and the
vasodilation or the widening of the peripheral skin becomes warm and flushed.
blood vessels which we remember is one of Distributive shock is a kind of
the components of vascular resistance. o If warm shock.
arterials dilate, vascular resistance to blood ▪ The overall combined effects of
flow goes down and blood pressure goes
widespread vasodilation,
down leading to less perfusion and
increased vascular permeability,
distribution of blood to organs and tissues. o and microvascular blood clotting
The most common type of distributive shock all contribute to decreased
is septic shock from pathogens in the blood. perfusion of blood to the vital
▪ What happens in septic shock is organs. o 2 subtypes of
that endotoxins (large lumpy distributive shock
lipopolysaccharides molecules
sometimes called as LPS’s) found ▪ Anaphylactic shock
in the outer membrane of gram •
negative bacteria causes a crazy • Allergic reaction
cascade of events that ultimately Causes dangerously low
leads to low perfusion. ▪ First, blood pressure
LPS damages the endothelial
cells and causes them to release
▪ Neurogenic Shock
vasodilators like nitric oxide. •
They also activate the Central
complement pathway in the nervous
blood which stimulates mast cell system gets
release of histamine (another damaged
vasodilator). The LPS molecules and cannot
also activate immune cells like control the
Macrophages and Neutrophils body’s blood
which help create a bunch of pressure.
proinflammatory cytokines like
Tumor Necrosis Factor (TNF) and •
Treatment of
Interleukin-1 (IL-1) which helps
the immune system destroy the Shock o
invaders but they also stimulate Depends on
the endothelial cells to release the cause
more inflammatory molecules o In general the goal is to stabilize the
like platelet activating factor and blood pressure so that vital organs such as
reactive oxygen species. the heart and the brain are perfused with
▪ All of these inflammatory blood. In order to stabilize blood pressure,
chemicals damage the fluid replacement and medications that
endothelial cells and increase increase heart contractility cause
their vascular permeability vasoconstriction and retain fluid can be
making the blood vessels leaky. administered. o Often times, a person might
Also, endothelial cells express a need supplemental oxygen or have their
procoagulant called tissue factor. airway protected.
Procoagulants are molecules that
increase blood coagulation/blood • Recap
clotting. This, in combination with o Shock is ultimately a failure in tissue
an overall decrease in perfusion
anticoagulants which usually
decrease clotting and seem to be

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 o It affects the whole body putting tissues • If all the cells will be damaged, it will later cause
and organs at risk for injury and ultimately tissue damage, that will lead to organ damage, to
organ failure. system failure
o Hypovolemic shock happens when
Pathophysiology of Shock Syndrome
dehydration or hemorrhage reduces the
volume of blood in the blood vessels. o
Cardiogenic shock happens when a direct
injury like a heart attack or an obstruction
like a pericardial effusion prevents the
heart from pumping blood efficiently.
o Distributive shock happens when
something like an allergic reaction or
damage to the nervous system
(neurogenic shock) causes the blood
vessels to vasodilate and become leaky
which reduces the resistance and lowers • How does anaerobic metabolism happen?
the blood pressure. o When cells are deprived of the essentials
that it needs, such as oxygen, products of
INTRODUCTION TO SHOCK (Recorded Lecture) metabolism switches from aerobic to
Shock •
anaerobic metabolism The main danger
• Inadequate organ perfusion to meet the tissue’s of having anaerobic metabolism is the
oxygen demand
•
production of lactic acid When the body
• Capacity of the body to provide good tissue
suffers from an outpouring production of
perfusion and to provide organs with oxygenated
•
blood for proper functioning o In tissue perfusion, lactic acid, cells tend to swell. This
remember that we need oxygen, blood, the causes cellular edema, therefore its
process of diffusion of oxygen and blood to function decreases and cells become more
become oxygenated blood. o And that •
permeable. Moreover, fluid electrolyte
oxygenated blood should be circulating in our
imbalance is imminent at this point.
body, providing perfusion to different organs for
proper functioning • If that happens and continuously happens without
further management, cells die and functions are
• Inadequate tissue perfusion due to one or more of
affected that later on would lead to system failure
the following cause: o Heart pump failure o Blood that leads to death
volume decrease o Arterial resistance
o Decrease venous bed capacity Stages of Shock
• Compensated/Early Shock: Body tries to
Effects of Shock [at a cellular level] reverse and counteract all the effects of a
decrease in blood volume/perfusion which causes:
o Vasoconstriction
▪ Renin & carotid sinus
baroreceptor o Increase in HR & RR
▪ Sympathetic activation o
Normotensive usually: to maintain normal
blood pressures
▪ Aldosterone/ADH Na+/ h20
retention)

• Suppresses release of water from the body

through the process of retention

• Decompensated/Late Shock: The body

• Cellular edema o If cellular edema happens, there manifests vital organ preservation so there is an
will be an increase in cell membrane permeability, increase in heart rate just to get the required
which causes the efflux and influx of sodium, oxygen demanded by the body. However, because
potassium, and water of lack of oxygen supply in perfusion, there is
worsening level of consciousness, and worsening
• Once the cellular edema progresses, the cells function of organs.
tends to be damaged causing mitochondrial
o Cool, clammy, hypotensive o Vital organ
swelling o Therefore, the cell cannot perform its
preservation o Worsening LOC o
function
Continued increase in HR and RR
▪ Cell - basic unit of life responsible ▪ Chemoreceptor response to
for body’s metabolism and metabolic acidosis
function

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 • Irreversible: The organs fail one by one leading ▪ Respiratory status is not that
to multiorgan failure, leading to death. good in the Irreversible stage
so that is
o HR and RR drop -> Multiorgan Failure ->
why the patient needs intubation
impending death
Assessment of Shock
• Assess Level of Consciousness o Most important
• Parameters that we need to check in
indicator of cerebral perfusion
Understanding how Shock develops: o Blood
pressure o Heart Rate o Respiratory Rate o • Watch out for increasing lethargy
• Monitor arterial blood pressure; if (+)
Condition of the skin o Urine output o Mentation compensation BP is elevated, decrease in BP may
o Acid-base balance occur in the late stage

STAGES OF SHOCK
• Narrowing pulse pressure o Evident in early in
shock
Finding Compensato Progressi Irreversible • Pulse quality is thready
ry ve
• Urine output is decreased o Check urine output
Blood Normal Systolic Requires
pressure <80-90 mechanical or
every hour o Check if patient is oliguria
mmHg pharmacologi (decreased urine)
c support • Capillary refill greater than 2 seconds
Heart rate >100bpm >150 bpm Erratic or • Skin is pale ashen gray, mottled cool and clammy
asystole
• Excessive thirst if intact LOC
Respirator >20breaths/ Rapid, Requires
y status mi n shallow intubation
Early Signs of Shock in Non Complicated Patients
respiration
s , crackles • Warm Early Stage/Pre Shock o Need high
Skin Cold, clammy Mottled, Jaundice index of suspicion because lack of signs
petechiae ▪ +/- tachycardia
Urinary Decreased 0.5mL/kg/h Anuric, ▪ +/- orthostatics (HR more
output r requires sensitive than BP)
dialysis
▪ +/- pulse pressure narrowing
Mentation Confusion Lethargy Unconscious
Acid-base Respiratory Metabolic Profound
▪ +/- restless
balance alkalosis acidosis acidosis • Hypoperfusion can be present in the absence of
significant hypotension o Don’t only rely on BP for
• From Compensatory to Progressive, it is evident diagnosing shock
that some of the parameters tend to be normal in
the compensatory stage. However, when in Signs of Late Shock Hypotension • Cold
reaches the progressive stage, there are slight
changes that signal management to counteract Late Stage o Cold, clammy and pale skin o
the effects of shock o One example of which is Rapid, weak, thready pulse o Rapid breathing
that the heart rate tends to increase by more than
150bpm just to produce the needed cardiac output
(blow off CO2 met acidosis) o Cyanotic o AMS
based on the oxygen demand of the body -> Coma
o Another example is the urinary output, o Anuria
wherein in the compensatory stage, there
will be a decreased urine output. However End Stage Clinical Effects (as shock progresses/worsens)
as the body progresses to the progressive • Cardiovascular o Myocardial depression o
stage of shock, urine output decreases by Vasogenic effects
0.5mL/kg/hr.
• Pulmonary o ARDS
• In the last stage, the Irreversible stage, wherein
• Renal o ARF
the systems will require assistance, be it through
mechanical or pharmacological • GI o Ischemic bowel
o Examples:
• Hepatic
▪ For blood pressure, we will be
o Increased LFTs, liver failure
requiring vasopressin;
▪ Heart rate is erratic in nature, • Hematologic o
Neutropenia, thrombocytopenia o
so there is a need to look into DIC (Gm- > Gm+)
the cardiac monitor and look
for arrhythmias and v-tach, • CNS o Coma
and without further
management will lead to Remember the following:
asystole;

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 • History and Physical are often limited by patient’s
condition o Ask and dig deeper on the history of • 4. Obstructive
the patient
▪ What are the underlying causes Disorders associated with the Different Types of

▪ What are the comorbidities ▪ Shock

What are the things that you • Cardiogenic o AMI, Cardiomyopathy, Valvular
need to get/ask so that we can Disease, Myocarditis, Arrhythmia
associate what the assessment
findings are, and figure out what • Hypovolemic
are the reasons behind that o Fluid loss, internal or external
manifestation
• Obstructive o Pneumothorax, Cardiac
• Patient presentation can be variable secondary to:
Tamponade, Acute PE
o Severity of the perfusion defect o
• Distributive o Sepsis, anaphylaxis
Underlying cause o Prior organ
dysfunction
• Examination should be tailored to be performed
quickly with highest yield for uncovering the cause
of shock o Shock is not a separate entity, but
rather a complication of its cause
▪ Meaning, whatever the underlying
cause is, when it hits the
complication level, shock is a
manifestation of that complication

Components (Fluids, Pump, Pipes)

• Blood (fluid) o Any change in the volume of the
blood will definitely affect perfusion, leading to
shock

• Heart (pump) o Anything that suppresses the

heart to perform its function, and any change in its
contraction will definitely affect one’s body and
progress to development of shock
Signs of Tissue Hypoperfusion (any of the shock can lead
• Blood vessels (pipes) o Any
to)
vasodilation/vasoconstriction will affect perfusion
levels that will also lead to • Brain o Altered mental state
development of shock
• Skin o Mottled, clammy
Types/Classifications of Shock • Kidney o Oliguria
• 1. Hypovolemic (fluids) o Significant fluid loss • Heart and Lungs o Tachycardia
from intravascular space may be due to
hemorrhage, burns, GI losses, fluid shift o Elevated blood lactate

o Any form of depletion that leads to a

Remember:
decrease in the circulating volume or that
supports the body circulation • Adequate circulating blood volume depends on 3
components
• 2. Cardiogenic (pump) o Pump failure
mechanism most common cause Myocardial
• A minor impairment in one can be compensated
for by the other 2 for a limited time
Infarction
o Any restriction of cardiac perfusion will • Prolonged or severe impairments will lead to shock
lead to cardiogenic shock
An Approach to Shock
o Any form of condition that will result in
pump failure or affect the contraction of • BP = SVR x CO o BP = blood pressure o CO =
the heart cardiac output o SVR = systemic vascular
resistance (pipes)
• 3. Redistributive/Circulatory (pipes) o Septic
▪ Results from accumulation of toxins • If the blood pressure is low, then either the:
and bacteria in the blood o CO is low, or
o Neurogenic o SVR is low, or o Both
▪ Brain hypoxia in origin o • Low SVR
Anaphylactic o There are only a few causes of low SVR.

▪ Caused by toxic allergic

reaction

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 They ALL cause vasodilation: ▪ Septic
shock ▪ Neurogenic (spinal cord
injury) shock
▪ Anaphylaxis shock
▪ Vasodilator (antihypertensive)
poisoning: overdose of
antihypertensives

• How do you assess SVR?

o Look at and feel the patient. o Low SVR
has the features:
• Blood pressure is affected by cardiac output and
systemic vascular resistance
▪ Warm
▪ Pink • Cardiac output is a result of stroke volume and
heart rate
▪ Bounding pulses ▪
Hyperdynamic heart (fast and • Stroke volume is affected by myocardial
pounding) contractility, preload, and afterload

• What if the SVR is high? o Pale

Why Monitor?
o Poor capillary refill (>2 seconds) o Cool
• Essential to understanding their disease
arm/legs (> 2 degree C difference) o
• Describe the patient’s physiologic status o Serial
Thready pulses (narrow pulse pressure:
monitoring
•
increase DBP) Cause of shock (low BP) is • Facilitates diagnosis and treatment of shock
then: Low CO
• What are the factors of CO? Monitoring Clinical Shock Parameter
o CO = HR x SV • Noninvasive o Blood pressure (SBP, MAP) o Urine
▪ CO = cardiac output output o Heart rate o Shock index
▪ HR = heart rate • Invasive o Pulmonary artery catheter (in the form
▪ SV = stroke volume o of Swan Ganz): CVP, PAWP, CO, SVR, DO2I,
Anything that is happening in SvO2 o Arterial catheter: ABP, Serum
heart rate and stroke volume, lactate, Base deficit
cardiac output will be affected

• HR Problems o Heart rate problems are easy to Diagnosis of Shock

diagnose o Rate: Bradycardia versus Tachycardia • MAP <60 or decrease of 20 from baseline
• Low SV (Stroke Volume) o Most • Systolic BP less than or equal to 90

• • Decreased systolic BP > 40mmHg from the

difficult to diagnose and manage patient’s baseline pressure

Stroke Volume depends on: o Preload - is the • Shock index (HR>SBP)

ventricle full? • Clinical signs & symptoms of hypoperfusion of
▪ Hypovolemic shock vital organs o Altered mental status, oliguria, cold
▪
Obstructive shock (i.e., Tension clammy skin, other forms of hypoperfusion
PTX,
Tamponade) o Mean Arterial Pressure
Cardiac Function • MAP is the mean perfusion pressure for the tissues
▪ Squeeze -> contractility - can the •
o Most required a MAP of 60 or greater
ventricle contract? Can blood get
Dependent only on the elastic properties of the
• arterial walls and the mean blood volume in the
out? -> valve function:
•
Normal? Regurgitation? arterial tree MAP = (2 x DBP) + SBP/ 3
Stenosis? Pulse
Pressure
Summary:
• SBP - DBP
• Perfusion (blood pressure) depends on:
o BP = CO x SVR o CO = HR x SV o SV = • The difference between the systolic (function of
ejection fraction) and diastolic pressures (function
preload and cardiac contractilityvalve of SVR and distensibility [elastic recoil] of the
aorta)
Components of BP Summary
• Wide:
o Normal 30-50 mmHg o Commonly seen
with fever, anemia, exercise and
hyperthyroidism
o AR (aortic regurgitation) is also a cause

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 • Narrow: ▪ Decrease gut perfusion
o May indicate an increase in vascular • Gastric tissue = esophagus = sublingual tissue ▪
resistance with decreased stroke volume Non invasive, hand held monitor
(i.e. aortic stenosis or decreased
intravascular volume)
▪ Rapid measurement ▪
Sensitive marker of decreased
blood flow
Additional

Invasive Markers Information:

Pulmonary Artery Catheter - an invasive equipment to
• Global Markers o Base deficit
know markers of shock
▪ Inadequate tissue perfusion leads
to tissue acidosis ▪ Amount of base
• Indications o Volume status o Cardiac status •
required to titrate 1L of whole arterial Complications o Technical o Anatomic
blood to a pH of 7.4 o Physiologic
• Normal pH level = 7.35 to
7.45
▪ Normal range: +3 to -3 mmol
per L
▪ Elevated base deficit correlates
with the presence and severity
of shock

• An increase in base deficit means that shock is

progressing, aside from
the fact that shock is
already present o
Lactate
▪ 1st part of the 1hr bundle is
getting the lactate levels and
determining
whether it is increased or
decreased
▪ Initial Lactate Standard Parameters
• The more lactate levels increases, the lower the • Measured o Blood pressure o Pulmonary A.
chances of survival • The presence of Pressureo Heart rate o Cardiac output o Stroke
hyperlactemia means that there is severity in volume o Wedge pressure
perfusion failure and the probability of survival is
very very low o CVP
• Calculated o Mean BP o Mean PAP o Cardiac
index o Stroke volume index o SVRI o LVSWI
o BSA

Goals of Shock Resuscitation

• Restore blood pressure
• Normalize systemic perfusion
• Preserve organ function

Parameters of Adequate Resuscitation

• Regional Markers o Gastric pH • Urine output (0.5 - 1.0 ml/kg/hr) o Acceptable
▪ Blood flow is not uniformly renal perfusion
distributed to all tissue beds • Reversal of lactic acidosis (nl. pH) o Improved
▪ Regions with inadequate tissue perfusion
perfusion may exist while global
markers are ‘normal’
• Normal mental status o Adequate cerebral
perfusion
▪ Gut mucosa among the first to be
affected during shock and the Shock is an Emergency
last to be restored to normal
• Goal: Rapidly restore Tissue Perfusion o Recognize
▪ Intramucosal pH falls when
it o Immediate stabilization: ABC
perfusion becomes inadequate •
A good determinant if perfusion • Shotgun approach
levels are good or not o Normalization of BP, pulse, UOP,
o Sublingual CO2

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 Hemodynamic parameters o Restoration
of aerobic metabolism, elimination of tissue
acidosis, repayment of O2 debt

• Treat the cause o Because shock is a symptom of

its cause
o In general, treat the cause

Management
• ABCs
o Maintain airway o Decrease work of
breathing & Optimize O2 o Circulation &
Control Hemorrhage includes:
▪ Direct pressure ▪
Pressure points ▪
Fluids & drugs Classes of Hypovolemic Shock

• Must address and treat: o Preload Class I Class II Class III Class IV
o Afterload o Pump (Irreversibl
e)
• Reassess every 5-15 minutes o The sicker the Blood <750 750-100 1500- >2000
patient, the shorter the interval Loss 2000
% <15% 15-30% 30-40% >40%
Management Priorities in Hypo perfused Blood
States Vol
Priori Physiolo Interventi Parame PAC Avoid Pulse <100 >100 >120 >140
ty # gy to on ter to targe Blood Normal Normal Decrease Decreased
improve target ts Pressu d
1 Volume Fluids CVP DO2 Low re
1015 SaO2 Pulse Normal Decrease Decrease Decreased
See Pressu d d
Chest re
xray Resp. 14-20 20-30 30-40 >40
2 Pressure Vasopres SBP 100 Low SV, Rate
sor or DO2 UOP >30 20-30 5-15 negligible
within Mental Sl. Mildly Confused Lethargic
High HR,
20-25 Status Anxious anxious
Resistan
torr ces Fluid Crystalloi Crystalloi Blood Blood
d d
MBP 80
of
•
patient’ As the classification increases, the
sN
parameters/measurements worsen o Blood Volume
3 Flow Inotrope Signs of DO2 Low BP,
lost in class 1 is 15%, on class 2 it’s 15-30%, class
perfusio SV,
3 30-40%, and class 4 more than 40%
n Resistan
ces o Resp rate increases because the body tries
to get the amount of oxygen it demands,
thereby an increase in RR
• BP Potency: Dopamine… NE..
Vasopressin/Phenylephrine
Clinical Signs of Acute Hemorrhagic Shock
• When in doubt, try a little more volume % Blood Loss Clinical Signs
< 15 Slightly increased heart
rate
TYPES OF SHOCK (Recorded Lecture)
15-30 Increased HR, increased
Types/Classifications of Shock DBP (narrow pp), prolonged
capillary refill, flat neck
•
1.HYPOVOLEMIC (FLUIDS) Significant fluid loss from veins
intravascular space may be due to hemorrhage, 30-50 Above findings plus
burns, GI losses, fluid shift hypotension, confusion,
acidosis, decreased
Pathophysiology of Hypovolemic Shock urine output
>50 Refractory hypotension,
refractory acidosis, death
• The higher the blood loss, the more clinical signs,
and the more critical the signs are

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

Causes of Hypovolemic Shock o Decreased left ventricular stroke work
• Hemorrhage (LVSW)

• Vomiting
Pathophysiology of Cardiogenic Shock
• Diarrhea

• Dehydration

• Third space
loss
• Burns

Signs of Hypovolemic Shock

• Decreased cardiac output
• Decreased PAOP/CVP
• Increased SVR

Treatment of Hypovolemic Shock

• Reverse hypovolemia & hemorrhage control
• Crystalloid vs Colloid o 1L Crystalloid = 250mL
Colloid
▪ Watch for fluid overload by •
From the decreased in cardiac contractility, the end
reassessing lung sounds ▪ portion will be a decrease in systemic tissue
3:1 Rule (3cc crystalloid for perfusion leading to heart failure, manifested by
1cc blood loss) pulmonary congestion, and worse will be deceased
▪ Watch for hyperchloremic coronary artery perfusion which will bounce back to
metabolic acidosis when large the heart,
volumes of NaCl are infused thereby decreasing its contractility property

▪ Best to give in 250mL boluses

Common Disorders that Lead to Cardiogenic
in
CHF followed by reassessment Shock
for another 250cc bolus •
Myocardial failure (MI)
o Colloids (ex: Albumin)
•
▪ Will increase osmotic pressure, Severe arrhythmia
watch for pulmonary edema •
Severe valvular dysfunction
▪ Remain in vascular space longer
(several hours)
Remember that Reduction in cardiac output leads to:
▪ Not increase survival > Decreased oxygen delivery
•
PRBC sooner than later Symptoms of Cardiogenic Shock
•
o 500mL whole blood increases Hct 2-3%, Skin:
250mL PRBCs increases Hct 3-4% o o Progressive peripheral vasoconstriction
Increases oxygen carrying capacity o Used results in cool, moist, pale skin with
with acute hemorrhaging (maintain Hct 24% mottling
and Hgb 8g/dL) •
Signs of Congestive Heart Failure o JVD,
• Not for Volume o FFP for coagulopathy (all HJR, APE, Pedal edema
factors) o Factor VII o PLT for •
thrombocytopenia Heart:
o Sounds: D/t enlargement and congestion
• Pressors
you can hear murmurs or S3 or S4

2.CARDIOGENIC (PUMP)
o Pulse: rapid rate and thready/weak pulse

• •
Pump failure mechanism most common cause BP: decreased BP and MAP
• •
Myocardial Infarction Any restriction of cardiac UO: decreases early due to decreased renal
perfusion will lead to cardiogenic shock perfusion that can lead to oliguria and anuria
Assess
•
Mech for:
o Defect in cardiac function (lost > 40% •
function) Signs of heart failure
•
• Signs o Decreased cardiac Signs of tamponade
output o Increased PAOP/CVP •
Cardiac dysrhythmia
o Increased SVR

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 •
Myocardial infarction o Tachycardia o Muffled heart
sounds or 3rd heart sound o Engorged neck veins
with hypotension o Dyspnea
o Edema in feet and ankles Pathophysiology of Distributive Shock

Treatment of Cardiogenic Shock

•
Increase oxygen supply to the heart
o Decrease O2 consumption (pain
meds/sedation)
o Increase O2 delivery (Mech vent, reperfusion
of the coronary arteries)
•
Maximize the cardiac output o Maintain normal
rhythm (dysrhythmics, pacing,
cardioversion)
o Diastolic vasopressors (dopamine,
epinephrine, norepinephrine, vasopressin)
o Improve myocardial contractility • It starts with vasodilation o Interaction of histamine
& bradykinin (inflammatory process)
▪ Inotropes (Dobutamine and
amrinone)
• A. Anaphylactic Shock
Decrease the afterload (workload of the left
•
ventricle) o IABP (Intraaortic balloon pump) o • Rapid onset Diffuse vasodilation mechanism
LVAD from histamine & bradykinin
The Failing
• Edema from increased capillary permeability o
Heart
This happens due to the vasodilation worsened
• by histamine & bradykinin
Improve myocardial function, CI <3.5 is a risk
factor, • Bronchoconstriction o WORST condition;
2.5 may be sufficient o Because if the heart fails, tightening of the airway that we need to
everything else will follow prevent

• • Symptoms
Fluids first, then cautious pressors
o Onset within seconds and progression to
• death in minutes
Remember aortic Diastolic pressures drives
coronary perfusion (DBP-PAOP = Coronary Perfusion ▪ Cutaneous manifestations: •
Pressure)
Urticaria, erythema,
• pruritus, angioedema
If inotropes and vasopressors fail, intra-aortic
balloon pump and LV assist devices ▪ Respiratory compromise

• Stridor, wheezing,
3.DISTRIBUTIVE/CIRCULATORY (PIPES) bronchorrhea, respiratory
distress
Types
• Septic ▪ Circulatory collapse
o Results from accumulation of toxins and • Tachycardia,
bacteria in the blood vasodilation, hypotension
• Neurogenic ▪ CNS
o Brain hypoxia in origin •
Apprehension -> AMS -> Coma
• Anaphylactic o Caused by toxic allergic reaction
•
Diagnosis o History and physical
Sig
alone make the diagnosis
ns
o Lab values serve no role
• +/- cardiac output
• +/- PAOP
▪ Histamine levels are elevated

• Decreased SVR
for about 30 minutes, tryptase for several hours•
Treatment o Remove the antigen o Treat ABCs
o IV Fluids, O2, Cardiac Monitor, Pulse ox o
First line Rx:

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 ▪ Epinephrine ▪ For severe o Monitor/findings:
bronchospasm, laryngeal ▪ Early: hyperglycemia, respiratory
edema, signs of upper airway alkylosis, hemoconcentration,
obstruction, respiratory arrest or
WBC typically normal or low
shock: IV Epi • 100
micrograms of
▪ Late: Leukocytosis, lactic
1:100,000 (place 0.1mL acidosis ▪ Very late:
of 1:1000 in 10mL of NS, disseminated intravascular
give over 5-10 mins) coagulation & multiorgan system
failure
▪ If less severe, can give 0.3-
0.5mL 1:1000 SC • Septic Shock Treatment o Prompt volume
o Second line: ▪ H1 blocker: replacement
Diphenhydramine 25- ▪ Fill the tank o Early antibiotic
50mg IV administration
▪ H2 blocker: Ranitidine 50mg or ▪ Treat the cause o If MAP <60
Famotidine 20mg IV ▪ Steroids ▪ Dopamine = 2-3
(Methylprednisolone 125mg IV microgram/kg/min
or Prednisone 40-60mg po)
▪ Norepinephrine = titrate (1-100
▪ Albuterol microgram/min)
▪ For patients taking beta-
blockers with refractory
hypotension, think One Hour Bundle for the Treatment of Shock
about glucagon
B. Septic
Shock
• Systemic Inflammatory Response (SIRS) o
Manifested by two or > of the following:
▪ Temp >38 or <36
centigrade
▪ HR > 90
▪ RR > 20 or PaCO2 < 32 ▪
WBC >12,000/cu mm or
>10% Bands (Immature
WBC)

• Septic Shock Trail o SIRS -> Sepsis ->

Severe Sepsis -> Septic
Shock o Sepsis is the combination of C. Neurogenic (Vasogenic) Shock
the Systemic Inflammatory Response •
Syndrome (SIRS) and a confirmed or Essential derangement:
presumed infectious etiology o Paralysis of the sympathetic chain which
o Severe Sepsis: SIRS criteria, source of controls vascular tone from injury to
infection and infection-induced organ thoracic or cervical level spinal cord injury
dysfunction or hypoperfusion ▪ There is no compensatory
abnormalities mechanism for neurogenic shock,
(sepsis + lactic acidosis/oliguria/AMS.etc) unlike in the other forms of shock
o Septic Shock: SIRS criteria, source of because there is paralysis in the
infection, and hypotension not reversed with sympathetic chain
fluid resuscitation and associated with organ o Produces decreased SVR from loss of
dysfunction or hypoperfusion abnormalities
vascular tone and bradycardia from
• Bacterial, viral, fungal infection unopposed parasympathetic input to SA
node
• “Warm Shock” is early stage o Fever,
tachycardia, tachypnoea, leukocytosis •
Caused by:
o Inadequate oxygen extraction (High SvO2, •
metabolic acidosis) in infected tissues o Spinal cord injury loss of SNS Massive
venous pooling & arteriolar dilatation •
• “Cold Shock” is late stage
Signs and symptoms:
• Septic/Inflammatory Shock o Signs: o Hypotension without tachycardia o Warm
▪ Early: warm w/ vasodilation, often
pink skin from cutaneous vasodilation o
adequate urine output, febrile,
tachypneic ▪ Late: vasoconstriction,
Low BP w/ minimal response to fluids o
hypotension, oliguria, altered mental Accompanying neurologic deficit
status

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 •
Spinal shock is not neurogenic shock o Spinal
shock: the temporary loss of spinal reflex activity
that occurs below a total or near total spinal cord
injury
•
Treatment o Increase vascular tone and improve
CO
▪ Increase preload with fluids

• CVP
• PAWP
▪ Increase vascular tone

• Vasopressors
▪ Maintain heart rate •
Treat bradycardia if
symptomatic
▪ Maintain adequate
oxygenation
•
Watch with SCI because of
the disruption of O2 to
the medulla
•
▪ Initiate therapy to prevent DVT
Sluggish venous flow
will increase risk factors
▪ Steroids (Methylprednisolone
30mg/kg over 15 min in first
hour, then 5.4 mg/kg/hr x 23
hours)

• There are contracting

studies, all of which
have flaw
o The symptoms of neurogenic shock
typically last 1-3 weeks
▪ Depending on the underlying
cause of neurogenic shock is the
prognosis

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 o
▪ The worse factors that may •
Vasopressor Agents o Augments contractility, after
happen will lead to poor
outcomes thereby poor prognosis preload established, thus improving cardiac output
o Risk tachycardia and increased
Nursing Goals for all the different Types of Shock myocardial oxygen consumption if used
• too soon
Compensatory - as much as possible, we need to
o Rationale: Increased CI improves global
reverse what we can reverse o Monitor tissue perfusion
perfusion o Reduce anxiety o Promote safety •
•
Vasopressors & Inotropic Agents o Dopamine
Progressive o Prevent complications o Promote Dobutamine o
rest and comfort o Support family members Norepinephrine o
• Epinephrine
Irreversible - prepare the patient and family by o Amrinone
family involvement, updates, and being open and
honest regarding the patient’s status
Fluid Replacement in Shock

General Medical Management

•
100% O2 by non-rebreather mask
•
Intubation if O2 management is adequate
• •
Fluid resuscitation Ringer’s lactate is the initial
fluid of choice.
o PNSS is the 2nd choice
•
Crystalloids and colloids
•
Packed RBC for massive blood loss SIRS – SEPSIS – SEVERE SEPSIS (Recorded Lecture)
• Systemic Inflammatory Response Syndrome
IFC insertion
(SIRS), Sepsis,
• Severe Sepsis
Patient on supine position with legs elevated
• •
ECG, ABG, CBC, and electrolyte Sepsis o Inflammatory syndrome from severe
infection
•
CVP insertion ▪ Vasodilation
• ▪ Increased WBCs ▪ Leakage
Main normothermia (in septic shock, patient should
be kept cool because fever increases, metabolic of fluid from capillary beds
• ▪ Remote from the site of
effects of shock) Vasopressors, inotropic agents
infection o Infection =
invasion of normally sterile
tissue by organisms
o Bacteremia = presence of viable bacteria
in blood
•
SIRS (Systemic Inflammatory Response
Syndrome) o Identical to sepsis but without
infection o Noninfectious process as a cause:
▪ Pancreatitis ▪
Modified Trendelenburg Position to aid in shock Autoimmune
disease ▪ Vasculitis
Vasoactive Agents used in Treating Shock ▪ Thromboembolism
▪ Burns
▪ Surgery/trauma ▪
Pulmonary
contusion

•
Definition of SIRS 2 or more of the
following abnormalities:o Temperature
(fever) o HR (tachycardia) o RR

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 o
(tachypnea) o WBC Count (high WBC •
More Organ Dysfunction Variables o Hemodynamic
count)
variables
• ▪ Hypotension
Note the lack of specificity o Example: Patients
with pulmonary edema •
SBP < 90 or
Pathophysiology of SIRS decrease > 40
• from baseline
Bacterial components from site of infection
•
• MAP < 70 o
Host immune response chemical signs from site of
Tissue Perfusion
infection Variables
• ▪ Elevated lactate ▪
Both enter the bloodstream o Vasodilatation and
Decreased cap refill or skin
changes in vascular autoregulation mottling
o Direct cellular toxicity
Possible Infection Markers
•
BP drops and perfusion decreases •
Procalcitonin level
•
Organ injury and dysfunction at sites away from •
TREM-1 receptor
the infection o Heart, lungs, kidneys, liver, brain,
•
coagulation cascade, etc CD64 expression on WBCs
•
Sepsis - Diagnostic Criteria Combination of these is best but still experimental
• o Procalcitonin level is becoming standard testing
Infection and some of these
o General variables Sepsis or SIRS?
•
▪ Temp >38.3 or <36 Early on, it may be hard to tell them apart
▪ HR >90 •
Look for a focus of infection somewhere o If found,
▪ RR >20
then sepsis o If none found, then SIRS o Cover for
▪ Altered mental status ▪ infection while looking for a source
Edema or positive fluid
balance ▪ 50% blood culture
(>20 ml/kg/24 hrs) positive in severe sepsis

▪ Hyperglycemia o ▪ 17% in sepsis ▪ 69% in

Inflammatory variables septic shock
▪ WBC Count >12,000 or
Sepsis Risk Factors
<4,000 ▪ Normal WBC Count
•
with >10% immature cells Nosocomial infection (antibiotics or ICU stay)
▪ C-reactive protein > 2 SD •
Bacteremia (positive blood cultures)
above normal
•
▪ Procalcitonin >2 SD above Age 65 or greater
normal •
Immunosuppression
• C-reactive protein & Procalcitonin
are markers o Cancer, renal/liver failure, AIDS,
of infection medications, splenectomy
•
Severe Sepsis - Diagnostic Criteria Diabetes
• Severe Sepsis: Sepsis and •
Community Acquired Pneumonia
•
Organ dysfunction Sepsis + •
Genetics
Organ dysfunction variables o
Hypoxemia (PaO2/FIO2 < 300)
Sepsis Epidemiology • US Estimate o 1.665 million
o Oliguria (urine < 0.5ml/kg/hr for 2 hours cases per year (and increasing)
despite a good fluid resuscitation)
•
o Creatinine increase > 0.5 (especially if > Older population (60-85% of cases)
2) o INR > 1.5 or aPTT > 60 secs o Ileus •
More immunosuppressive meds
(no bowel sounds) o Thrombocytopenia •
(plt < 100,000) o Elevated bilirubin > 4 More antibiotic resistance

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 • o Central venous
Maybe better detection
lines
•
Highest incidence is African American males •
Site of Infection Correlates Prognosis o Sepsis
•
Highest in winter (Respiratory infections/flu)
w/ UTI = lowest mortality (26-30%) o Unknown, GI,
•
Pathogens o Gram positive bacteria pulmonary (50-55% mortality)
▪ Staph (think MRSA, o GI (ischemic bowel) - 78% mortality
Sepsis
MSSA) ▪
Treatment
Strep •
(Pneumonia, and Usage of one-hour bundle
Group A o Check lactate level o Have blood culture
Beta) taken

▪ C. Diff •
Fluids
▪ Enterococcus
•
o Gram negative bacteria (E. coli, klebsiella, Treat infections o Antibiotics o Surgical drainage
pseudomonas, citrobacter, enterobacter, •
etc.) Supportive Care o Correct physiologic
o Fungal (increasing but still lower abnormalities (Hypoxia, BP)
incidence) •
Distinguish between sepsis and SIRS
•
Severity increasing (more cases severe sepsis) o
ARDS, acute renal failure, DIC Early Management
Sepsis •
ABCs o Oxygen
Prognosis
o Monitor pulse ox o Consider intubation
•
High mortality rate (10-52%) o Increases with and mechanical ventilation
severity ▪ Decrease work of breathing
▪ SIRS - 7% ▪ Airway protection for decreased
▪ Sepsis - 16% mental status
▪ Severe sepsis •
- 20% Diagnostics
▪ Septic shock o ABG
- 46% o Lowest in young o Chest x ray o Labs including cultures
(<44 y/o) and those with
•
fewer chronic diseases Correct decreased tissue perfusion o Monitor BP
• frequently o Consider arterial line monitoring, if BP
Poor Prognostic Factors o Hypothermia (or
unstable
failure to spike a fever o Leukopenia (especially ▪ Hypotension is most common
with gram negative) o Coagulation abnormalities sign
▪ Elevated INR and aPTT ▪ Other signs include tachycardia,
decreased capillary refill,
▪ Decreased functional fibrinogen
decreased mental
levels
status/restlessness, decreased
o Elevated chloride level o Elevated lactate
urine output ▪ Modified by
(>4) = 78% mortality preexisting conditions or meds
•
Comorbidities = Poorer Prognosis o New onset • I.e Beta blockers o
Follow lactate levels
atrial Fib o AIDS
o Liver disease o Cancer o Alcohol Fluid Management
dependence o Immunosuppression o Age • Venous Access ASAP o
> 40 May need a central line
▪ Chronic illnesses ▪ Fluids, pressors, blood
▪ Impaired immunity products

▪ Malnutrition ▪ Blood draws

▪ Exposure to resistant ▪ Central venous pressure

organisms ▪ Central venous oxygen
• Nursing homes saturation o Pulmonary artery
catheter (Swan Ganz)
• Medical devices o
Indwelling catheters ▪ No longer routinely used

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 o
• CvP and ScvO2 give similar ▪ Once perfusion restored, not
findings helpful unless it begins to rise
again
• More complications

• IVFs (Crystalloids) o May need 2- Summary:

5 over 6 hours (500mL boluses) •
Whether protocols, early goal directed therapy or
o Careful if history of CHF o
Assess volume status, perfusion, usual care is given o Fluid resuscitation should
BP, and signs of pulmonary begin within 6 hours
edema or ARDS ▪ Stopped or reduced when
o Fluid overload is common perfusion restored

▪ Monitor •
Antibiotics given expeditiously when it appears that
responsiveness/perfusion and don’t
infection is present/worked up
continue once
improvement stops •
If perfusion deficit/organ failure progresses o
Fluid and Med Choices Reassess adequacy of fluids, antibiotics, need for
surgical care, accuracy of diagnosis, complications
•
Crystalloid is best - 1st line therapy o No •
When patient responds, back off of support but
differences with Albumin (higher cost) o Others
(starches) may increase mortality monitor the markers for sepsis (BP, UO, labs, etc) o
Reevaluate if worsening or not continuing to
•
Pressors - 2nd line therapy o For hypotension once improve
fluid status is
improved Dealing with the Focus of Infection
o Norepinephrine preferred (both alpha and •
Identify the site of infection o Info from history &
beta)
Phenylephrine, if tachycardia or physical o Blood culture 2 sites, aerobic and
arrhythmias anaerobic o Urine cultures, sputum cultures and
▪Pure alpha agonist o Gram stain
Dopamine has fallen out of favor o CSF o CXR
o Infected line, indwelling catheter, site of
Med Choices - Conflicting Evidence
injury in trauma patient
•
Inotropes (Dobutamine) - 3rd line o For myocardial
dysfunction once BP Infectious Site of Infection
improves •
Early, appropriate antibiotics after cultures o
o Increases cardiac output/tissue perfusion
Started within 6 hours (prefer 1 hour) o Consider
o Raise CvO2 sat > 70 o May worsen recent antibiotics, comorbidities, and possibility of
hypotension hospital/health care acquired infection
• Late/inadequate/inappropriate
Blood transfusion to optimize Oxygen delivery o antibiotic = poor outcome
Hemoglobin < 7 (unless bleeding or myocardial
ischemia) Infectious Source Unknown
o No longer performed with hgb 9 •
Broad Spectrum Antibiotic Coverage o Staph
Aureus (and MRSA)
Early Goal Directed Therapy
• ▪ Vancomycin is the 1st line ▪
IVFs given in the first 6 hours using physiologic Daptomycin, linezolid, Ceftaroline
targets to guide management 2nd line o If Pseudomonas is
o Widespread acceptance but best targets unlikely, add 1 of these
aren't known (conflicting evidence) ▪ 3rd of 4th generation
o MAP > 65 (and probably >80) o Urine Cephalosporin (Cefepime)

output > 0.5ml/kg/hr o Radial pulse ▪ Beta lactam/beta-lactamase inhibitor

(Pip-tazo)
showing respiratory variation o CvP 8-12 ▪ Carbapenem (Imipenem)
(if central line placed) o ScvO2 > 70 (if o If pseudomonas is possible, add 2 of the
central line placed) o Follow lactate levels previous
q6 hr until falling ▪ List could also include Ceftaz,
(maybe as good as ScvO2) Quinolone (Ciprofloxacin),

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 Aminoglycoside (Gent), or does not rise or fall, there is no
Aztreonam mechanism of respiration

• Process of Dying
Infectious Focus Present
•
Drainage/debridement/amputation of site of 1. Sequential Loss of Life Functions o If a patient
infection o May not respond to antibiotics alone went to arrest; initially the body would stop, the
doctor would order a code to revive the patient, if
• the code is successful, the patient may be revived
Remove potentially infected foreign bodies o
Central line, urinary catheter with some limitations but definitely there is some
loss of functions in the body. o Example: sense of
Monitor Improvement sensation, sight
• •
Narrow the antibiotic spectrum when cultures and 2. Terminal Apnea = Last breath o Cheyne-stokes
• respirations is
sensitivities return Watch for antibiotic toxicity,
evident: waxing and waning movement of
response, superinfection the chest (gasping)
(hospital acquired)
•
• 3. Agonal State = “death rattle” = noise, liquid,
Duration of Antibiotics: 7-10 days o Longer if
bubbling o Sphincters are relaxing; liquid and
response is slow, immunologic deficiency,
undrainable focus, or secretions are coming out of the body
neutropenic (until neutropenia resolves) •
4. Clinical Death = No pulse, No breath
Additional Therapies •
5. Brain Death = No central nervous activity o
•
Steroids (Glucocorticoids) o Treat host Coma = life activities only continue with the aid o f
machines
inflammatory response o Most likely to help
hypotensive septic shock unresponsive to fluids & o Coma = associated with a person not
pressors responding to anything and that because
of the aid of machines and supports such
• as mechanical ventilators and certain
Nutrition o Helps conserve body weight and
drugs, the patient is able to have vitals of
muscle
life and can be termed “living”
mass
o May not change clinical outcomes
Speed of Death
• •
Venous thromboembolus prophylaxis o Reduces Instantaneous = instant death (explosion) o
risk of DVT/PE Cardiac arrest o Trauma o Accidents
•
Intensive Insulin o Hyperglycemia and insulin •
Acute = fairly rapid (gunshot)
resistance are
common and promote infection •
Result of shock = body shuts down (heart attack,
o Target blood glucose 140-180
no blood to cells) o Body shuts down due to
• volume/perfusion problems
Fever control w/ antipyretics (Acetaminophen) o
o The organs fail thereby making the body
•
Potential benefits and adverse effects External prone to death
cooling - unclear benefit o May lower mortality, •
Progressive dying = illness with death in days,
decrease pressor requirement, etc
months, years (Cancer)
DYING AND DEATH (Recorded Lecture)
Recommendation A.1: Minimum Clinical Criteria
Medical/Legal Definition for NDD
• (Neurological Determination of Death)
Criteria for “Brain Death” o Bilateral (both eyes)
dilated (open), and fixed (unresponsive) pupils We recommend use of the following minimum clinical

o Voluntary and involuntary reflexes gone o criteria as a Canadian medical standard of NDD:

Can’t breathe without a machine o No •

Established etiology capable of causing
heart activity o No brain waves o All of neurological death in the absence of reversible
which must be supported by diagnostics; conditions capable of mimicking neurological death
for example, in terms of heart activity, the •
ECG shows asystole; for the brain waves, o Should be irreversible in nature Deep
the EEG shows absence of brain functions; unresponsive coma with bilateral absence of motor
for the eyes, the simple use
responses, excluding spinal reflexes o Bilateral
of penlight would show that both the eyes
unresponsiveness
are dilated and unresponsive, absence of
PERLA; using the Apnea test, the chest

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 o
• the patient is dead because they collapsed. There is a
Absent brainstem reflexes as defined by absent reversible cause that can be managed declaring the patient
gag and cough reflexes, and the bilateral absence as ROSC or Return Of Spontaneous Circulation
of o Corneal responses •
Hypothermia (core temperature less than 34
o Pupillary responses to light, with pupils at
degrees celsius)
mid-size or greater
o Vestíbulo-ocular responses •
Severe metabolic disorder capable of causing a
• potentially reversible coma o Glucose, E+ (PO4,
Absent respiratory effort based on the apnea test
Ca, Mg), IEM, LFT, creatinine, BUN
•
Absent confounding factors (that could be ▪ Should correct any abnormality
reversible) that could possibly influence
decision
o Hypoglycemia
Overarching Recommendations
•
• Peripheral nerve/muscle or NMJ (neuromuscular
NDD = Neurological Determination of Death o
Confirmation of NDD = legal time of actual death junk) blockade • Drug intoxications o ETOH,
barbiturates, sedatives, hypnotics
▪ Even if there is intact cardiac
functions (assumed this will ▪ Should calculate 5 ½ lives to clear
be temporary, and non- drug; longer if cooled
sustained) o NB therapeutic levels of AED, sedatives or
o When a patient is pronounced as dead, we analgesics do not preclude the diagnosis
have met all the criteria necessary for a
patient to be pronounced dead. Irreversible Cause of Death
▪ We do not pronounce the patient •
Neurological assessments may be unreliable in the
as dead if they are gasping, or
there are still impulses. acute post-resuscitation phase after
cardiorespiratory arrest. In cases of acute hypoxic-
• ischemic brain injury, clinical evaluation for NDD
No clear medical basis for 2 independent exams o should be delayed for 24 hours subsequent to the
Can be performed by 2 MD’s concurrently o If cardiopulmonary arrest or an ancillary test could be
performed at different times, a full clinical performed.
examination, including apnea testing, must be Even if there are reversible causes, even if
performed at each determination there is management provided, look
carefully at the outcome. Example, in
o No fixed interval of time is recommended cases of acute hypoxic ischemic brain
for the second determination, except injury, you need to evaluate the NDD
where age-related criteria apply effectively. If the patient is revived after
• CPR, you need to examine if the patient
Aetiology established that can cause irreversible still has the pulse, is the patient breathing,
death is there ROSC? If yes, then you cannot say
that the condition of the patient is
o No confounders
reversible, you cannot pronounce the
• patient as dead even if the patient is still
Deep coma unconscious.
o Absence of motor responses to stimuli, no
spontaneous or abnormal movements
(dyskinesia, posturing) or
•
seizures o N.b. spinal reflexes may Core temperature must be greater than or equal to
exist 34 degrees celsius to proceed with formal testing.

• o Central blood, rectal or esophageal-gastric

Absence of brainstem reflexes o No spontaneous
breathing during apnea test o Previously was 32.2 degrees celsius

• Brain Death Exam

Infants (greater than or equal to 30 days and less
than 1 year); repeat exam recommended •
Pupils o Greater than or equal to 4-9mm,
unresponsive to light (inquire about Rx given)
Rule Out these Confounders (reversible cause of a
patient’s deep coma/unresponsiveness; can be •
treated to reverse the condition and make patient Corneals o Movement of jaw or lids excludes NDD
fall under the category of “living”) • Un- •
Vestíbulo-ocular responses o OCR (Doll’s Eyes;
resuscitated shock o If a patient went to arrest, the arrest oculo-cephalic)
can be treated with resuscitation so we cannot just say that
▪

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 ▪ Caution if trauma ▪ ▪ PCO2 40+/-
Mechanical/gravitational forces 5mmHg o
stimulate vestibular responses Disconnect
▪ Normal response = ventilator
eyes always gaze up towards ▪ T-piece with CPAP
roof at 10cm H2O,
▪ Rapid, but steady movements deliver FiO2 at
10L/min or insert
and observe for direction of
catheter into ETT
gaze • Activates vestibular and deliver FiO2 at
system ipsilateral to head thrust 6L/min (at level of
(same principle for HIT) carina)

• Communicates with o Observe for respiratory efforts x 8-10 mins

contralateral horizontal o Repeat ABG at 8-10 min and reconnect
gaze center (CN VI) ventilator
“orchestrating” the
▪ Test + if
action of the eyes
•
• Simultaneously dampens PaCO2 is greater than or
contralateral vestibular equal to 60 mmHg and
tone etc. rise in 2 mmHg/min
(greater than or equal to
20 mmHg) above
baseline levels and pH
less than or equal to 7.28 •
o Cold calorics No respiratory efforts
▪ 30 degrees to the horizontal demonstrated • Stop if HD
instability or desaturation
▪ Minimum if 50cc of ice cold water
occurs
into the inner ear canal • Ensure
no perforated tympanic o Carefully remove the patient from the
membrane before instilling water mechanical ventilator and look whether
• the patient will have a rise or fall of chest
Use kidney basin, prop up and later on determine the ABGs of the
beside ear patient

▪ Start observing for eye deviation o If severe lung disease

rapidly; eye movements should ▪ Caution must be exercised in
be absent for 1 minute considering the validity of the
▪ Minimum of 5 minutes before apnea test
evaluating contralateral side ▪ If in the physician’s
▪ Cold Stimulation - opposite judgement, there is a history
reaction of the eyes suggestive of chronic
respiratory insufficiency and
▪ Warm calorics - same side responsiveness to only
reaction supranormal levels of carbon
If i instill cold water into the right dioxide, or if the patient is
ear, expect that the movement dependent on hypoxic drive
of both eyes will go to the left; if
you inject warm water to the ▪ If the physician cannot be
right ear, expect that the eyes sure of the validity of the
will roll apnea test, an ancillary test
towards the site of injection should be
administered
▪ Thermal energy stimulates Ancillary
vestibular responses
Testing
•
Pharyngeal o Stimulate posterior pharynx o •
The term ancillary should be understood to mean
Suction the ETT o Depress larynx, swallow reflex o alternative test to one that otherwise, for any
Swallowing reflex or none reason, cannot be conducted o No longer called
• “confirmatory” or
Apnea test o Temperature greater than or equal to
“supplemental” o
34 degrees celsius, SBP greater than 90 mmHg Different connotations
(adults), euvolemia o Pre-oxygenate with •
Gold standard - global absence of intracerebral
100% FiO2 for 10-15 mins
(PaO2 greater than 300 mmHg) blood flow (only 2 tests support) o Cerebral
o Baseline ABG angiography or radio-isotope scan

▪ pH: 7.35-7.45

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 o
•
Ancillary testing:
o Should be performed when any of the
minimum clinical criteria cannot be
established or confounding factors remain
unresolved

•
Specialists with skill and knowledge in the
management of newborns with brain injury and the
determination of death based in neurological
criteria

•
Special Circumstances Children greater than or
equal to 1 year (including adolescents)
o Same criteria
o Mandates a second exam
▪ No fixed time interval o
Physician qualified with working with
critically ill children (ex. Not an adult
neurology resident doing an elective at
the MCH)

•
30 days to 1 year old (corrected for GA) o Minimum
clinical criteria = OCR (more reliable due to
external auditory canal anatomy)
o Repeat exam recommended by another
physician/at another time (lack of
collective experience and research on
brain death in this age group)
o If uncertain or confounders factoring in,
extend time interval or perform ancillary
testing
o Specialists with skill and knowledge in
management of infants with severe brain
injury

NDD recommendations for term newborns aged

•
<30d Standards apply for all those greater than 36
weeks gestation

•
NDD is clinical o Absence of OCR and suck reflex o
Temp (core) greater than or equal to 36 degrees
celsius

• •
Min time from birth to determination is 48h 2
determinations required, minimum interval 24h

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

Other tidbits
•
NDD can be determined (in adults) o Any physician
licensed by the college of physicians and surgeons
or licensing authority in that jurisdiction
o Exclues physicians who are only on
education register
o Does not require a particular level of
specialty certification;
o Nonspecialists can declare NDD if they
have the requisite skill and knowledge

Organ Donation
•
3 pronged approach o Environment ▪ Caring
attitude; be open and honest
▪ Ask if family members around, or
if there is a family spokesperson
▪ Take family to a private room ▪
Offer pastoral services
▪ Offer phone, tissue, etc. o
Knowledge
▪ Assess loved-ones
comprehension of the situation ▪
Emphasize irreversibility of brain
death
▪ Repeat the information as many
as necessary
▪ Grant enough time to assimilate
the new knowledge
▪ Grant enough time to assimilate
the new knowledge
o The Question (at a future time-point)
▪ Verify wish of deceased (organ
donor signature on RAMQ card)
▪ Be attentive to apprehension;
answer questions +++
▪ Offer possibility of
communication with T-Q
▪ Emphasize possibility of giving
the gift of life to another

Figures/Important Images

Ways to Determine Time of Death

•
Eye witnesses
•
Diagnostics (ECG, EEG)

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 • •
Hours o Degree of digestion of stomach contents B. Bloated Stage (Day 2-6) o Putrefaction
and test bodily fluids begins. Gasses produced by anaerobic bacteria
inflate the abdomen.
•
Algor Mortis o The change in body temperature o o The body starts to smell
Falls at about 1.5 degrees celsius per hour o The •
C. Decay Stage (Days 5-11) o Abdominal wall
body is cooler/colder o Science of Algor Mortis
breaks - gasses escape - carcass deflates
▪ No more heat generating
chemical reactions •
D. Post-decay Stage (Days 10-25) o In dry
▪ No more homeostasis by brain of habitats, remains are skin, cartilage, and bones. In
body temperature ▪ Diffusion of wet habitats, wet viscous material in the soil under
heat until at equilibrium with the remains.
room temperature
•
▪ Faster in windy conditions and in E. Dry Stage (Days 25+) o Mainly bones and
water hair remain. Odor is primarily that of normal soil
and litter. Can last several months to years.
▪ Children and thin people cool
faster
Loss, Death and Grief
• Kubler-Ross Stages of Grieving
Livor Mortis
•
o Settling of red blood cells; this reddens Denial
the skin •
Anger
o Begins within ½ hour, most evident within
12 hours - after that, liver mortis will not •
Bargaining • Depression
move regardless of how the body is
moved •
Acceptance
o Science of Livor Mortis
▪ Heart stops ▪ Vessels Rando Categories of Response

breakdown ▪ Red blood cells

•
Avoidance
are dense and settle according to
gravity in body
•
Confrontation o When death sinks in
(as a result: hyperbilirubinemia
will surface making jaundice •
noticeable until such time the
Accommodation o When you have fully accepted
patient is pale in color) death

▪ Pressure moves blood cells Can Clinical Symptoms of Grief

see if body has been moved after •
death • Rigor Mortis Signs and symptoms of stress reaction •
Board-like stiffening in about 12 hours, Normal manifestations o Verbalization of the loss
lasts another 12 hours, and releases in o Crying o Sleep disturbance o Loss of appetite o
another 12
hours Difficulty concentrating • Complicated grieving o

o Science of Rigor Mortis Extended time of denial o Depression o Severe

physiologic symptoms
▪ No blood pumped
o Suicidal thoughts
▪ No oxygen to muscles ▪
Bacteria doing anaerobic •
respiration Measures that Facilitate the Grieving Process
▪ Make lactic acid ▪ Low pH Explore and respect ethnic, cultural, religious, and
causes actin and myosin to personal values
contract muscles, so they •
Teach what to expect in the grief process
stiffen until ATP gone and
fibers decompose •
Encourage the client to express and share grief
▪ Stiffening begins at jaw and •
migrates down with support people Teach family members to
encourage the client’s expression of grief
Stages of Decomposition •
• Encourage the client to resume activities on a
A. Fresh Stage (Days 1-2) o Commences at schedule that promotes physical and psychological
death, ends when bloating is first evident. health
Breakdown of protein and carbohydrates into
simpler compounds Help Clients Die with Dignity

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 o
• •
Introduce options available to the client and Apply additional identification tags
significant others to restore and support feelings of •
control: Wrap the body in a shroud
o Location of care o Times of appointments •
Apply identification to the outside of the shroud
with health professionals
•
o Activity schedule o Use of health Take the body to the morgue or arrange to have a
mortician pick it up from the client’s room
resources o Times of visits from relatives
and friends o Assist clients to manage •
Handle the deceased with dignity
the events preceding death so they can
die peacefully •
Empathy over sympathy
o Helps client to determine their own
physical, psychological and social DEATH AND DYING NOTES (Additional Reading;
priorities PPT)
o Support the client’s will and hope

Strategies to Facilitate Discussions about Death

•
Identify personal feelings about death
•
Focus on client’s needs
•
Determine client’s usual ways of coping
•
Establish communication relationship
•
Determine what client knows about illness
•
Respond with honesty and directness
•
Make time to be available

Assisting Families of Caregivers of Dying Clients

•
Use therapeutic communication
•
Provide an empathetic and caring presence
•
Explain what is happening and what to expect
•
Have a calm and patient demeanor
•
Hearing is the last sense that can disappear
•
Encourage to participate in the physical care as
they are able:
o Assist with bathing o Speak or read to the
client o Hold hands
Death
• •
Support those who feel unable to care for or be The final stage of growth
with the dying o Show an appropriate waiting area •
if they wish to remain nearby Experienced by everyone
•
• The young ignore its existence
May be therapeutic for the family to verbally give
permission to the client to “let go” when ready •
The old begin to think of their own
•
After the Client Dies Death imposes two kinds of burdens:
• o 1. Preparing oneself for one’s own death
Encourage the family to view the body
• o 2. Deal with the interpersonal aspects
May wish to clip a lock of hair as a remembrance of death that will affect one’s loved ones
• ▪ Grief, anguish, anger, anxiety,
Children should be included in the events
surrounding the death if they wish denial

After Body Viewed by the Family Societal Meanings of Death

• •
Leave wrist identification tag on Modern American o Medical failure

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 • •
More traditional societies o Natural part of life Living longer than expected
cycle •
Coming to terms with finitude
US: Societal Changes - early 1900s and now •
Dealing with the deaths of friends
•
Early 1900s o Focus was on comfort o Died of
infection o Died at home o Family was caregiver o Dying Process
Death was short and sudden •
Stages of Death and Dying (Elizabeth Kubler Ross,
• 1960: 200 Terminally Ill)
2005 o Focus is on cure o Die of chronic illness o
Die in institutions o Institution staff are caregivers o Denial: Not me! o Anger: Why me? Why

o Death is prolonged
now? o Bargaining: Yes, me....but! o
Depression: Yes...me… o Acceptance: Yes,
Cultural Views on Death me.
•
Eastern philosophies-death is natural Bereavement
• •
Buddhists and Hindus o Physical death is rebirth Older adults undergo much bereavement
(reincarnation) •
o End of rebirths that is their goal, not the Widowed men (up to age 75) are almost twice as
end of death which is the goal of likely to die than married men
Chrisianity
•
o Oneness with the universe; Focus is not Grief: reaction to loss (Lindemann, 1944) o Upset
on the self stomach o Shortness of breath o Tightness in
• throat o Sighing o Decreased muscular strength
Western-death is to be postponed, threat
•
Grieving practices vary (Rituals) o By culture:
The Issue of Dying Across the Life Span weeping/partying
• o By ethnicity: wake/shiva
Childhood o Until around 5-7 don’t understand
the permanence, universality, and lack of
Reaction to loss: Grieving Practices
functioning in death
•
o Age 12 accurately perceive Rituals - Jewish o Funeral: begins with cutting
▪ Parent euphemisms (just went to away” (black ribbon or garment)
Shica (7 days after burial): parents,
sleep)
children, spouses and siblings of the
▪ Attending funerals deceased, preferably all together in the
• deceased’s home
Adolescence o More experienced with death and
o Mourners sit on low stools or the floor
grief o Loss of sibling, friend or parents (survivor’s instead of charis
guilt)
▪ Do not wear leather shoes
o Positive outcomes includes greater
▪ Do not shave or cut their hair
appreciation for life
▪ Do not wear cosmetics
•
Adulthood o Middle-aged ▪ Do not work ▪ Do not do things
for comfort of pleasure (bathe,
▪ Understand next in line to die
have sex, put on fresh clothing)
▪ Change in perception of time o Mourners wear the clothes that they tore
(lived vs. amount left) at the time of learning of the death or at
the
• Death of a parent funeral
• Death of a child -
violates the natural
o Mirrors in the house are covered o
order “Baruch dayan emet”, blessed be the one
true Judge
▪ Transition to being the oldest
generation
Rituals
• •
Late Adulthood (Older o
Adults) Least Wakes/visitations o Viewing of body (70-80%) o
concerned with dying o Loss of a partner o Loss of Social gathering o Reading a will and executing it
a child or grandchild
o Wearing black
o Although think about death more

Who are the primary caregivers of dying people?

Why not Afraid?
•
• Their child: 35%
Goals have been fulfilled

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 o
• Designed for situations in which the individual is in
Their spouse: 30% a coma and cannot express his or her desires
•
Their sibling: 9% •
Many states have natural death legislation
•
Their parent: 9% •
People engaged in end of life planning are more
• likely to:
Someone else: 16%
• o Have been hospitalized in the year prior
75% of the time, these people are female
o Believe that patients rather than
physicians should make healthcare
Who loses a spouse? decisions
o Have less death anxiety o Have survived
Age: 65-74 Age: 75-84 Age: 85+
the painful death of a loved one
Women 36% 62% 80%
Men 9% 19% 43% •
Euthanasia: the act of painlessly ending the lives of
individuals whoare suffering from an incurable
Common Ideal Death Scenarios disease or severe disability o Passive euthanasia:
• treamtent is withheld o Active euthanasia: death
Sudden death in sleep (older adults too)
deliberatley
•
Dying at home induced
• •
Dying engaged in meaningful activity Trend is toward acceptance of passive euthanasia
•
Themes for a “Good” Death in the case of terminall ill patients Experts do
• not agree on the boundaries or mechanisms by
Home which treatment decisions should be implemented
• •
Comfort Active euthanasia was made famous by Dr. Jack
• •
Sense of completion (tasks accomplished)
Kevorkian in the US as “assisted suicide” Active
• euthanasia is a cimr in most countries and in the
Saying goodbye
• •
US (except Oregon) Patients who have a
Life-review
• desire for euthanasia are often: o Less religious o
Love
Have been diagnosed with depression o Have a

LIFE-SPAN DEVELOPMENT TWELFTH EDITION: DEATH,

•
lower functional living status Hospice: a
DYING,
program committed to making the end of life as
AND GRIEVING (Additional Reading; PPT)
free from pain, anxiety, and depression as possible
The Death System o Palliative care: reducing pain and suffering,
• helping individuals die with dignity
In most societies, death is not viewed as the end of
existence because the spiritual body is believed to o Makes every effort to include the dying
live on patient’s family members

• o Includes home-based programs today,

People in the US tend to be death avoiders and supplemented with care for medical
death deniers needs and staff
• •
Changing Historical Circumstances o The age Family members report better psychological
group in which death most often strikes adjustment to the death of a loved one when
o Life expectancy has increased from the 47 hospice care is used
to 78 years •
A good death involves physical comfort, support
o Location of death
from loved ones, acceptance and appropriate
medical care.
Issues in Determining Death
Advance Directive & Living Wills
•
Brain death: a person is brain dead when all
electrical activity of the brain has ceased for a
specified period of time o Includes both the higher
cortical functions and the lower brain-stem function

Life, Death, and Health Care

•
Advance directive & living wills are designed to be
filled in while the individual can still think clearly o

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 Context in Which People Die
•
More than 50% of Americans die on hospitals
• •
Nearly 20% die in nursing homes Hospitals offer
many important advantages: o Professional staff
members o Technology may prolong life
•
Most individuals say they would rather die at home
Grievi
ng
•
Attitudes Toward Death Greif: emotional numbness, disbelief, separation
• anxiety, despair, sadness, and loneliness that
Death of a parent is especially difficult for children
accompany the loss of someone we love o Grief is
• a complex, volving process with multiple
Most psychologists believe that honesty is the best
dimensions
strategy in discussing death with children o
Depends on the child’s maturity level o More like a roller-coaster ride than an
orderly progression of stages
•
Terminally ill children may distance themselves •
from their parents as death approaches Cognitive factors are involved in the severity of
•
• grief Good family communications and grief
Most adolescents o Avoid the subject of death
counselors can help grievers cope with feelings of
until a loved one or close friend dies
separation and loss
o Describe death in abstract terms and
have religious or philosophical views
•
Prolonged grief: approximately 10%-20% of
about it survivors have difficulty moving on with their life
o Often think that they are somehow after 6 months have passed
immune to death •
Disenfranchised Grief: an individual’s grief
•
Concerns about death increases as one ages: involving a deceased person that is a socially
ambiguous loss that can’t be openly mourned or
o Awareness usually intensifies in middle
supported
age
o Examples: ex-spouse, abotriton,
▪ Middle-aged adults often fear stigmatized death (such as AIDS)
death more than young adults or
older adults •
Dual-Process Model o Loss-oriented stressors:
o Older adults are more often preoccupied focus on the deceased individual
by it and want to talk about it more
▪ Can include grief work and both
o One’s own death usually seems more positive and negative reappraisal
appropriate in old age, possibly a of the loss
welcomed event, and there is an o Restoration-oriented stressors: secondary
increased sense of urgency to attend to stressors that emerge as indirect
unfinished business outcomes of bereavement

Kubler-Ross’ Stages of Dying ▪ Changing identity and mastering

new skills
•
Denial and Isolation: “It can’t be me” o Effective coping involves cycling between
• coping with loss and coping with
Anger: “Why me?”
restoration.
•
Bargaining: “Just let me do this first!” •
Impact of death on surviving individuals is strongly
•
Depression: “Withdrawal, crying, and grieving” influenced by the circumstances under which the
• death occurs o Traumatic, violent, or sudden
Acceptance: “A sense of peace comes” deaths are likely to have more intense and
prolonged effects
Perceived Control and Denial
▪ Can be accompanied by PTSD-
•
Perceived control may be an adaptive strategy for like symptoms
• •
remaining alert and cheerful Denial Cultural Diversity o Some cultures emphasize the
insulates and allows one to avoid coping with importance of breaking bonds with the deceased
intense feelings of anger and hurt and returning quickly to autonomous with the
deceased vary extensively
o Can be maladaptive depending on extent

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

 o
o Beliefs about continuing bonds with the kidneys will be activated by conserving fluid o Causing
decreased vary extensively a decrease in urine output
o There is no one right, ideal way to grieve •
Heart and Lungs are the core workers when body
Losing a Life Partner undergoes shock o Heart - the last one to “give
• up”
Widows outnumber widowers 5 to 1 o Women live
•
longer than men o A widowed man is more likely to 15 minutes without oxygen in the brain (hypoxia)
remarry o Widows usually marry older men will lead to brain dead

• Synchronous Lecture (09/04/2021)

Widowed women are probably the poorest group in
America •
Respi alkalosis - due to rapid breathing
• (compensatory)
Women tend to do better than men because
women typically have better networks of friends •
and relatives Turning point: Progressive Stage
o Older women do better than younger •
Crackles are present in the Progressive Stage
women
because of fluid accumulation in the lungs due to
• beginning organ failure and change in pressure in
Religiosity and coping skills are related to well-
capillaries causing fluid leakage o Crackles a sign
being following the loss of a spouse in late
of left sided heart failure
adulthood
•
Irreversibile - last stage of shock o We only can do
Forms of Mourning damage control
•
Approxiamtely 80% are buried; 20% are cremated •
Inotropic Effect - main effect is how the force of
• contraction will be changed
Funerals are an important aspect of mourning in
many cultures •
Chronotropic Effect - how fast or how regular your
• heart will beat
Cultures vary in how they practice mourning
•
SHOCK (Synchronous Lecture 09/03/2021) Jaundice - connected to liver failure
•
• Hypovolemic shock - fluid
A complication or a sign of an underlying disorder
•
• Cardiogenic shock - pump
Keyword: Body doesn’t meet the demand for good
•
perfusion Distributive shock - pipes
o Perfusion needs oxygen & oxygenated
blood circulating around the body Hypovolemia
•
• Origin: low blood volume
Cell: basic unit of life
•
• Caused by: o Hemorrhage o Burns
1st response of the body when undergoing shock is
to reverse it, which is the 1st stage of Shock •
Treatment: Replace fluid
“Compensatory”
•
• Crystalloids:
5 Vital Organs:
o Brain - level of consciousness o Heart - o Lactated Ringers or PNSS o Albumin -
for delivery & circulation of oxygenated water magnet
•
blood; reflects heart rate o Lungs - CVP - reflection of fluid status
respiratory rate
Kidneys - filters & excretes toxins; controls 3 Classical Signs of Asthma Wheezing, Dyspnea, Cough
balance of fluid; reflected by the urine
output Themes for a Good Death
o Capillaries (Peripheral System) - blood • Home
vessels, for delivery of oxygen & blood; • Comfort
reflected by blood pressure • Sense of completion (tasks accomplished)
• • Saying goodbye
1st organ/body system that first reacts when the
• Life-review
body undergoes shock: Capillaries (Peripheral
System) o So that the circulation will go from • Love

• 1st sense that the patient will loss: Sight as manifested by

periphery to central After periphery, the
dilation

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT

Last sense that the patient will loss: Hearing

NCM 118 LEC TRANS/NOTES #4 | AAA & ARMDT