Alexander ch17 lecture

Copyright © 2017, 2012 Pearson Education, Inc. All Rights Reserved.
Advanced EMT
A Clinical-Reasoning Approach, 2nd Edition
Chapter 17
Resuscitation:
Managing Shock and
Cardiac Arrest

• Applies fundamental knowledge of the causes,
pathophysiology, and management of shock,
respiratory failure or arrest, cardiac failure or
arrest, and postresuscitation management.
Advanced EMT
Education Standard

1. Define key terms introduced in this chapter.
2. Identify situations in which you should withhold
resuscitative attempts.
3. Explain each of the links in the Chain of Survival
of cardiac arrest.
4. Explain the importance of early defibrillation in
cardiac arrest.
5. Explain the importance of high-quality chest
compressions CPR.
Objectives (1 of 5)

6. Describe the features, functions, advantages, limitations,
use, and precautions in the use of automatic external
defibrillators (AEDs).
7. Compare and contrast ventricular fibrillation, ventricular
tachycardia, asystole, and pulseless electrical activity.
8. Describe safety precautions to protect yourself,
other EMS providers, the patient, and bystanders
in resuscitation situations.
Objectives (2 of 5)

9. Given a series of cardiac arrest scenarios involving
infants, children, and adults, demonstrate appropriate
assessment and resuscitative techniques, including the
integrated use of CPR, AEDs, airway management, and
ventilation.
10.Explain the purpose and procedure for reassessing
patients in shock and cardiac arrest.
11.Given a cardiac arrest scenario, make decisions
regarding transport and a request for paramedic backup.
12.Demonstrate assessment and management of a
post–cardiac arrest patient with return of spontaneous
circulation (ROSC).
Objectives (3 of 5)

13.Explain the importance of AED maintenance, EMS
provider training and skills maintenance, medical
direction, and continuous quality improvement in the
Chain of Survival of cardiac arrest.
14.Discuss special considerations in the use of an AED
in patients with cardiac pacemakers and implanted
cardioverter–defibrillators.
15.Discuss the use of mechanical CPR devices.
16.Demonstrate effective methods for controlling external
hemorrhage.
Objectives (4 of 5)

17.Discuss the indications, contraindications,
complications, and administration of intravenous
fluids to patients in cardiac arrest and hemorrhagic
shock.
18.Discuss current trends and research in resuscitation and
shock management.
Objectives (5 of 5)

• Shock, respiratory failure and arrest, and cardiac
failure and arrest all result in inadequate perfusion
to maintain cellular metabolism.
• Prehospital care priority
– Restore conditions for aerobic cellular metabolism
• Series of interventions
– Resuscitation
Introduction (1 of 2)

• When resuscitation required
– Understand resuscitation priorities.
– Focus on priorities of situation.
– Have well-practiced skills.
– Apply skills critically to meet patient’s immediate
needs.
– Requires teamwork.
– Review each resuscitation situation.
Introduction (2 of 2)

Think About It
• What should Mary and Grace anticipate as
possible causes of cardiac arrest?
• How should they prioritize their interventions once
they arrive at the scene?
• What factors are likely to affect the patient’s
outcome?
• What can Mary and Grace do to influence those
factors?

• Shock
– Result of physiological insult that threatens
cellular perfusion.
– Compensatory mechanisms exist, but they
are limited.
– Without medical intervention to restore perfusion,
the patient will die.
Pathophysiology of Shock (1 of 20)

• Hypoperfusion
– Perfusion is adequate when cells receive blood
supply needed to provide oxygen and nutrients for
metabolism and to remove metabolic wastes
– Perfusion requires adequate:
 onloading of oxygen in red blood cells
 transportation of red blood cells to tissues
 offloading of oxygen for use at the cells

• Hypoperfusion (continued)
– Conditions needed for perfusion
 Heart functions as pump
 Blood vessels provide peripheral vascular resistance through
vasoconstriction
 Sufficient volume of blood with adequate oxygen-carrying
capacity

• Hypoperfusion (continued)
– Initial stages of shock
 Signs and symptoms reflect body’s attempts at
compensation
– Later stages of shock
 Signs and symptoms reflect consequences of
inadequate tissue perfusion

Figure 17-1
Mechanisms of shock.

• Mechanisms of shock
– Hypovolemic
– Distributive (vasogenic)
– Cardiogenic
– Obstructive
– Respiratory/metabolic

Table 17-1 (1 of 3)
Comparing and Contrasting Types of Shock
Type of Shock Description and
Pathophysiology
Signs and Symptoms Management
Hypovolemic Fluid loss from dehydration or
burns, or blood loss results in
decreased vascular volume.
The body attempts to maintain
cardiac output and perfusion
by increasing heart rate and
peripheral vascular resistance.
Early signs and symptoms
include thirst; anxiety; slight
tachycardia; cool, pale skin;
and slight tachypnea. As
shock progresses, the patient
becomes diaphoretic,
hypotension occurs,
tachycardia and tachypnea
increase, and mental status
changes (confusion, agitation,
decreased responsiveness).
Ensure an open airway,
adequate ventilation, and
oxygenation. For hemorrhagic
shock, control external
bleeding. Consider the need
for fluid replacement in the
prehospital setting. Transport
to the nearest hospital
capable of providing the care
that the patient needs.

Table 17-1 (2 of 3)
Type of
Shock
Description and
Pathophysiology Signs and Symptoms Management
Distributive Blood volume is
normal but cannot be
distributed throughout
the body for perfusion
because the capacity
of the vasculature is
increased. Causes
include sepsis,
anaphylaxis, and loss
of sympathetic
nervous system
regulation of
vasoconstriction.
Anaphylactic shock: There may be a history of
exposure to an antigen (bee sting,
medications, etc.), or the patient may have
edema, dyspnea, hives, vomiting, abdominal
cramps, or diarrhea. The airway may be
obstructed by edema, and wheezing may be
present. The patient is tachycardic and
hypotensive. Mental status decreases in
response to hypoxia and hypoperfusion. The
skin may be mottled rather than pale, and the
patient may be diaphoretic.
Septic shock: The patient may have a history
of infection or have risk factors for infection,
such as a Foley catheter or intravenous
access. The patient is hypotensive and usually
tachycardic, with altered mental status. The
skin may be cool and mottled, and the patient
may be hypothermic.
Neurogenic shock: Occurs in the context of
high spinal-cord injury. The patient is
hypotensive, but skin is warm and dry, and
heart rate is normal. Mental status may be
impaired, but often perfusion is not profoundly
affected.
Ensure an open airway and
adequate ventilation and
oxygenation. In the prehospital
setting, fluids may be beneficial to
increase vascular volume.
However, the overall need is to
return the size of the vascular
container to normal. This can be
achieved in anaphylaxis by the
administration of epinephrine,
which causes vasoconstriction.
In septic shock, administer
intravenous fluids and manage the
patient’s body temperature,
keeping in mind that he may have
a fever or may be hypothermic.
In neurogenic shock, assess for
accompanying hemorrhagic
shock, based on the mechanism
of injury. With spinalcord injury
above C5, the diaphragm is
impaired and the patient may
require positive pressure
ventilation.

Table 17-1 (3 of 3)
Type of
Shock
Description and
Pathophysiology Signs and Symptoms Management
Cardiogenic There is a problem with the
heart, such as muscle death
from myocardial infarction
(death of 40 percent or more
of the left ventricle), heart
failure, or an abnormal heart
rate decreases cardiac
output.
May have signs and symptoms of
ACS (chest pain or discomfort,
dyspnea, nausea, vomiting); signs
of pulmonary edema (crackles
[rales], dyspnea); pale, cool,
diaphoretic skin; altered mental
status (confusion, syncope,
decreased responsiveness);
systolic blood pressure
< 90 mmHg; varied heart rate
depending on underlying cause;
jugular venous distention; or
cardiac dysrhythmia.
In addition to managing the
airway and providing oxygen,
ventilation may be improved in
patients with signs of pulmonary
edema through the use of CPAP.
Assist or provide positive
pressure ventilations if
necessary. IV fluids may help
increase preload and increase
cardiac output, but may also be
poorly tolerated by patients with
heart failure. Consult with
medical direction concerning
fluid administration.
Obstructive There is a mechanical
obstruction to blood flow,
such as a pulmonary
embolism, tension
pneumothorax, or cardiac
tamponade, that decreases
venous return to the heart
(preload).
The onset of signs and symptoms
may be abrupt and may include
severe dyspnea, altered mental
status, hypotension, tachycardia,
and jugular venous distension.
In tension pneumothorax, breath
sounds are decreased or absent
initially on the injured side but later
on both sides.
Manage the airway, ventilation,
and oxygenation. IV fluids may
temporarily increase preload, but
the underlying cause must be
corrected.

• Hypovolemic shock
– Results from absolute decrease in vascular volume;
common in prehospital setting
– Results from medical or trauma condition
– Hemorrhagic shock
 Significant blood loss
 Results in overall volume loss and loss of oxygen-carrying
capacity

• Hypovolemic shock (continued)
– Nonhemorrhagic hypovolemic shock
 Body fluids lost from
– excessive vomiting or diarrhea
– inadequate fluid intake
– extensive burns
– loss of fluid into interstitial spaces

Figure 17-3
The cycle of hemorrhagic shock.

– Hemorrhagic shock
 Decreased cardiac output
 Decreased blood pressure
 Sympathetic nervous/renin-angiotensin systems activated
 Renin-angiotensin system prevents further fluid loss; causes
vasoconstriction

– Diaphoresis
– Anxiety
– Peripheral vasoconstriction decreases circulation to
skin (pale, cool skin; thready peripheral pulses).
– Blood pressure remains normal as long as significant
fluid loss not ongoing.

Figure 17-4
(A) Normal microvascular perfusion. (B) Peripheral capillary beds are bypassed in
response to sympathetic nervous system stimulation.

• Hemorrhagic shock
– Four progressive classifications of hemorrhage
 Based on amount of blood lost
 Signs and symptoms
– Three physiological phases of shock
 Compensated, decompensated, ireversible
– Three tissue phases of shock
 Ischemic, stagnant, washout

Table 17-2
Classification of Hemorrhage
Class Blood Volume Loss
in a 70-kg Adult
Signs
Class I
hemorrhage
Up to 15 percent
(750 mL)
Usually well tolerated
Can lead to mild
Tachycardia
Class II
hemorrhage
15–30 percent
(750–1,500 mL)
Moderate tachycardia
Pale skin
Delayed capillary refill
Class III
hemorrhage
30–40 percent
(1,500–2,000 mL)
Tachycardia
Failure of compensation
Hypotension
Class IV
hemorrhage
40–50 percent
(2,000–2,500 mL)
Profound hypotension
End-organ failure (e.g., bradycardia, anuria)
Death

Table 17-3 (1 of 2)
Compensated and Decompensated Shock
COMPENSATED SHOCK
Sign Physiological Explanation
Anxiety Response to epinephrine from sympathetic nervous system response (fight-or-
flight reaction)
Normal blood pressure Peripheral vasoconstriction shunts blood away from capillary beds and increases
peripheral vascular resistance; heart rate increases to maintain cardiac output
Tachycardia (100–120 per
minute)
Decreased stimulation of baroreceptors results in increased heart rate via
sympathetic nervous system stimulation of the SA node
Pulse quality (thready in
extremities, becoming weak)
Vasoconstriction shunts blood away from extremities
Slight to moderate tachypnea
(20–30/min)
Increased stimulation of respiratory center in medulla in response to increased
PaCO2 and decreased PaO2
Pale, cool skin; moist skin Vasoconstriction in response to epinephrine and norepinephrine from sympathetic
nervous system to divert remaining volume from nonvital to vital areas of the
body

Table 17-3 (2 of 2)
Compensated and Decompensated Shock
DECOMPENSATED SHOCK
Sign Physiological Explanation
Altered mental status (agitation,
confusion, decreased
responsiveness)
Cerebral hypoperfusion
Hypotension Blood loss exceeds ability of compensatory mechanisms
(>30 percent blood volume loss); failure of compensatory
mechanisms due to hypoxia and acidosis
Marked tachycardia (>120;
at 140 and above, patient’s
circumstance is dire); may
progress to bradycardia
Continued response to hypotension; bradycardia as heart becomes
hypoperfused and fails
Pulse quality (weak, becoming
absent)
Reflects continued decrease in volume and cardiac output insufficient
to produce pulses
Air hunger (tachypnea;
[>30/minute]/hyperpnea);
progresses to respiratory failure
Acidosis, hypoxia.
Skin (white, waxy, cold) Absence of peripheral perfusion, decreased heat production due to
inadequate metabolism

Table 17-4
Ischemic, Stagnant, and Washout Phases of Shock
Ischemic Phase Stagnant Phase Washout Phase
Selective vasoconstriction shunts
blood flow away from capillary beds,
causing tissues served by those
capillary beds to become ischemic.
The precapillary sphincter of the
arteriole leading into the capillary
bed and the postcapillary sphincter
of the venule leaving the capillary
bed are both constricted.
The affected tissues must use
anaerobic metabolism, resulting
in acidosis.
Progressing hypoxia and acidosis
result in failure of the precapillary
sphincters. Blood enters the
capillary bed, but the postcapillary
sphincter remains constricted.
Blood stagnates in the capillary
beds.
Shock is considered irreversible
at this point.
Further hypoxia and acidosis
cause the postcapillary
sphincters to fail. Accumulated
acids and microemboli formed
in the capillary beds are now
released into the circulation,
worsening acidosis.

• Ischemic phase
– Peripheral tissues do not receive adequate perfusion
 Perfusion restored quickly; shock reversible at this stage.
 If shock not corrected, lack of energy and decreased
pH cause precapillary sphincters to fail.

• Stagnation phase
– Blood cells clump together
• Washout phase
– Results devastating, leading to additional tissue
and organ damage

• Once critical number of cells of any organ die,
organ fails; irreversible shock.
– In some cases, death occurs immediately.
– May die hours or days later from
 ARDS
 MODS
 DIC

Figure 17-5
Distributive shock is caused by vasodilation and increased capillary permeability.

• Distributive shock
– Normally, both sympathetic and parasympathetic
nervous systems control the diameter of blood vessels.
– When pathologic state results in excessive
vasodilation, blood pressure decreases, resulting in
hypoperfusion.

• Anaphylactic shock
– Anaphylaxis
 Severe allergic reaction.
– Can lead to airway edema and obstruction,
vomiting, diarrhea
– Widespread, systemic vasodilation
– Loss of fluid into interstitial spaces, reducing
vascular volume

• Septic shock
– Occurs due to combined effects of body’s aggressive
response to massive infection and effects of pathogen
itself.
• Neurogenic shock
– Result of impaired sympathetic nervous system
function.

• Distributive shock signs
– Septic and anaphylactic shock
– Tachycardia; diaphoretic
– Neurogenic shock
 Blotchy, mottled skin; warm, dry skin; normal heart rate despite
hypotension

Figure 17-6
Cardiogenic shock from myocardial infarction.

• Cardiogenic shock
– Heart’s failure as pump reason for inadequate
perfusion.
– Physical damage of myocardium reduces ability of
heart to contract.
– Function of heart impaired; hypotension occurs.

• Cardiogenic shock (continued)
– Electrical conduction abnormal.
– Bradycardia can result in decrease in blood pressure.
 Heart does not contract frequently enough to maintain
pressure in vascular system.
– Tachycardia (rates over 150) not enough time for
ventricular filling.

• Obstructive shock
– Mechanism creates obstruction to blood flow that
cardiac output significantly diminished.
– Causes
 Pulmonary embolism, cardiac tamponade, tension
pneumothorax
– Gas exchange cannot occur.
 Produces hypoxia and hypercarbia
– Blood cannot get past obstruction.

Assessing for Shock (1 of 7)
• Anticipate shock; actively look for indications.
• In all cases, there is some indication of
hypoperfusion.
• Consider shock in differential diagnosis of patients
with tachycardia.

• Scene size-up
– Look for hazards.
– Assess need for additional resources.
– Determine number of patients.
– Determine MOI or nature of illness.
– General impression
 Obvious bleeding, pale or mottled skin, decreased level
of responsiveness, and respiratory distress

• Primary assessment
– Airway, breathing, circulation.
– Ensure open airway, adequate ventilation,
oxygenation.
– Anticipate vomiting.
– Control external bleeding with direct pressure.
– Confirm level of responsiveness.

• Primary assessment (continued)
– Determine if breathing present.
– Use manual maneuvers, suction, airway adjuncts
as indicated.
– Confirm initial impression.
– Establish priorities for treatment.
– Transport.

• Secondary assessment
– Patients in shock (medical or traumatic causes)
receive rapid physical examination.
– Assess baseline vital signs.
– Apply monitoring devices.
– Obtain medical history.
– Perform head-to-toe physical exam.

• Clinical reasoning
– Determine likely underlying cause of shock.
– Determine treatment beyond primary assessment.
– Physical exam clues important.
– Goal of treatment
 Interrupt progression toward decompensation and
irreversible shock

• Reassessment
– Patients with shock can deteriorate rapidly.
– Reassess level of responsiveness, airway, breathing,
oxygenation, circulation, effects of interventions.

Managing Bleeding and Shock (1 of 13)
• Untreated shock leads to death.
• Without intervention, progressive deterioration
and death inevitable.
• Best treatment is to prevent it.
• In the case of Blood loss, simple interventions
may be effective in preventing shock.
• Early recognition and interventions may improve
chances of survival.

• Bleeding control
– Stop further external bleeding.
 Direct pressure
 Tourniquet
 Topical hemostatic agent
– Internal bleeding
 Requires surgical intervention
– Transport patient to best source of definitive care.

Figure 17-8
Steps of hemostasis.

Figure 17-9
Types of bleeding.

• Hemostasis
– Vessels constricts, narrowing vessel and reducing
blood flow.
– Platelets from injured vessel attracted to injured area;
adhere together to form platelet plug.
– Coagulation cascade transforms platelet plug into
stable fibrin clot.

Table 17-5 (1 of 3)
Medications and Supplements That May Affect
Blood Clotting
Medication/Supplement Use Effects on Hemostasis
Apixaban (Eliquis) An oral anticoagulant that acts by
inhibiting a clotting factor. Prescribed for
patients with atrial fibrillation and to treat
or prevent deep venous thrombosis
(DVT) and pulmonary embolism (PE)
Prevents formation of a stable fibrin clot
aspirin Over-the-counter analgesic and anti-
inflammatory; used to inhibit platelet
aggregation in patients at risk for ACS
Reduces ability of platelets to clump
together to form a platelet plug
clopidogrel (Plavix) Prescription platelet aggregation inhibitor Reduces ability of platelets to clump
dabigatran (Pradaxa) A prescription oral medication used to
inhibit thrombin in patients who have or
who are at risk for DVT or PE
Prevents formation of a stable fibrin clot
dipyridamole (Persantine) Prescription platelet aggregation inhibitor Reduces ability of platelets to clump
dong quai Herbal supplement taken for many
conditions, including menopausal
symptoms
Herbal and dietary supplements can
reduce blood clotting on their own, or
they may interact with antiplatelet and
anticoagulant drugs to increase the risk
of bleeding

Table 17-5 (2 of 3)
Blood Clotting
edoxaban (Savaysa) An oral anticoagulant that acts by
inhibiting a clotting factor; prescribed
for patients with atrial fibrillation and
to treat or prevent deep DVT and PE
Inhibits clotting factor Xa, which interferes
with the blood clotting cascade
feverfew Taken for migraine headaches Herbal and dietary supplements can reduce
blood clotting on their own, or they may
interact with antiplatelet and anticoagulant
drugs to increase the risk of bleeding
fish oil Taken for its omega-3 fatty
acids, which reduce the risk of
cardiovascular disease
Herbal and dietary supplements can reduce
garlic Taken in concentrated form
(oil, extract, capsules) for anti-
inflammatory effects on immune
system and to reduce the risk of
cardiovascular disease
gingko biloba Taken to improve memory and
concentration

Table 17-5 (3 of 3)
Blood Clotting
ginseng Taken to relieve fatigue and stress
and to enhance sexual and mental
performance
heparin An injectable anticoagulant that
interferes with the blood clotting
cascade; prescribed for a variety of
conditions in which blood clotting may
be Increased
Formation of fibrin clots is impaired
Rivaroxaban (Xarelto) An oral anticoagulant that acts by
inhibiting a clotting factor; prescribed
for patients with atrial fibrillation and
to treat or prevent DVT and PE
Inhibits clotting factor Xa, which interferes
with the blood clotting cascade
warfarin (Coumadin) Oral anticoagulant that interferes with
the clotting cascade; prescribed for a
number of conditions in which blood
clotting may be increased
Formation of fibrin clots is impaired

Figure 17-11
Direct pressure controls most external bleeding.

• Direct pressure
– Place sterile, absorbent dressing over wound and
apply firm pressure until bleeding controlled.
– Secure dressing in place using pressure dressing.

• Topical hemostatic agents
– Chemical and physical agents
– Adjunct to direct pressure
– Chitosan, zeolite, and kaolin-based products
– Follow protocols

Figure 17-13
A commercial tourniquet.

• Tourniquets
– Bleeding severe and ongoing despite direct pressure,
apply tourniquet.
– Wide band applied
 constrict both venous and arterial blood flow.
– Extremity wounds are treated by placing tourniquet
between wound and heart.

• Tourniquets (continued)
– Do not cover; must be clearly visible at hospital.
– Can be painful; analgesia should be considered.
– Transport patients who have tourniquet applied to
highest level trauma center available.

• Extremity elevation/arterial pressure points
– Use of pressure points not recommended.
– Elevating extremity is no longer recommended as a
method of bleeding control.
– Follow your protocols.

• Intravenous access and fluid administration
– IV fluids during transport.
– Critical thinking about potential consequences:
 Blood dilution
 Decreases oncotic pressure
 Loss of clotting factors
 Increase blood pressure
 Hypothermia

• Intravenous access and fluid
administration (continued)
– There is no way to control internal bleeding in the
prehospital setting
– Externally accessible bleeding, infuse intravenous
fluids to increase blood pressure
– Permissive hypotension
 Maintain systolic 80–90mmHg by administering 500cc of
isotonic crystalloid fluid
 Suspected increased intracranial pressure with hemorrhagic
shock—target systolic 90–100 mmHG

• Fluid resuscitation in nonhemorrhagic shock
– Best treated by reversing underlying cause.
– Know pathophysiology of various types of shock.
– Septic and anaphylactic shock have distributive and
hypovolemic components.
– In anaphylaxis, administration of epinephrine causes
vasoconstriction; fluids adjunct to treatment.

• Fluid resuscitation in nonhemorrhagic
shock (continued)
– In septic shock, patient may be dehydrated from
underlying infection.
– In cardiogenic shock, patient may not be able to
handle additional fluid load without developing
pulmonary edema.
– In obstructive shock, fluids can increase preload and
increase cardiac output and blood pressure.

• Pneumatic anti-shock garments (PASGs)
– Trousers with inflatable compartments.
– Use may complicate some conditions.
– Application can interfere with treatments that have
higher priority in management of shock.
– Follow local protocols.

Think About it
• What additional information do Mary and
Grace need for the employees who responded
with the AED?
• As the team leader, what does Grace need
to communicate to her team, and how should
she communicate it?
• How does the information about the HPI affect
your ideas about the underlying cause of cardiac
arrest and the patient’s chance of survival?

Cardiac Arrest (1 of 37)
• Sudden cardiac arrest (SCA)
• Acute coronary syndrome (ACS)
• Other causes
– Dysrhythmias, trauma, hypothermia, drug
overdose, electrolyte imbalance, toxins, stroke,
and pulmonary embolism
• Rare in children; result of respiratory failure

• Heart develops dysrhythmia; does not produce
mechanical contraction sufficient to generate
cardiac output.
• Perfusion ceases; patient becomes pulseless,
unresponsive, and apneic.
– Pulseless rhythm
 Ventricular fibrillation, ventricular tachycardia, asystole,
pulseless electrical activity (PEA)

• Body tissues and organ systems rapidly
damaged by lack of perfusion.
– Brain and heart are extremely sensitive to ischemia
• Cellular death in four to six minutes.
• Death in 8 to 10 minutes if perfusion not
restored.

• The Chain of Survival
– Immediate recognition and activate 911
– Early, high-quality CPR
– Rapid defibrillation
– In-hospital advanced life support and post–cardiac
arrest care, cardic catheterization, and intensive
care unit

• Cardiopulmonary resuscitation
– Lay rescuers
 Taught unresponsive patient with absent or abnormal
breathing requires immediate initiation of 30 chest
compressions.
 Unable to distinguish between who has pulse and who
does not.
 Should not delay chest compressions to check for pulse.

Figure 17-16
(a)
(A) If a carotid pulse is not detected in 10 seconds, begin chest compressions.

• Health care provider CPR
– Quickly check patient’s carotid pulse.
– If pulse not detected within 10 seconds, begin chest
compressions.
– Advantage by responding in teams.

• Scene size-up and primary assessment
– Unresponsive patient (cyanotic or mottled skin)
 Immediate need to resuscitate
– Cardiac arrest not immediately apparent
 Quickly check for responsiveness, breathing, pulse
– If unresponsive and has apnea or agonal respirations,
quickly check carotid pulse.
– If you do not detect carotid pulse in 10 seconds, begin
chest compressions.

• Chest compressions
– Once arrest recognized
 Compressions started
– Sequence of patient care
 Cardiac arrest identified; circulation, airway,
breathing (CAB)

• Chest compressions (continued)
– Certain amount of oxygen in blood and lungs but an
ideal amount is not being circulated.
– Time taken to assess, establish airway, and perform
bag-valve-mask ventilations delays circulation of blood.
– Creates both negative and positive intrathoracic
pressure to alternately fill heart with blood and squeeze
it out into circulation.

Figure 17-18
Hand placement for adult chest compressions.

– Push hard and fast. Limit interruptions.
– One provider begins chest compressions while another
prepares defibrillator.
– If alone, perform chest compressions until another
provider arrives.
– Compress 100–120 compressions per minute:
30 compressions to 2 ventilations until advanced
airway placed.
– Minimize interruptions.

– Mechanical CPR devices useful tool in case of
prolonged CPR or where manpower scarce.
– Follow manufacturer’s instructions.
– Adhere to your protocols.

Figure 17-20
Open the airway and begin ventilations after 30 chest compressions.

• Airway and ventilations
– Open airway and deliver ventilations by
bag-valve-mask device or mouth-to-barrier mask.
– Deliver each ventilation over one second using
enough volume to obtain visible chest rise.
– Resume compressions.
– If air does not enter despite proper airway position,
suspect foreign body airway obstruction (FBAO).
– Treatment for FBAO is chest compressions; check
to see if object dislodged.

• Airway and ventilations (continued)
– Vomiting can occur; ensure suction available to clear
airway.
– Advanced airway in place, chest compressions
delivered continuously at 100–120 per minute and
ventilate every 6 seconds
– Rotate provider performing chest compressions.

Figure 17-21
(A)
(B)
Automatic external defibrillators.

• Defibrillation
– Early defibrillation critical for patients in pulseless
ventricular rhythm.
– The greater the interval between arrest and the start
of resuscitation, the poorer the chance of survival.
– To maximize successful defibrillation, keep chest
compression interruptions to minimum.

• Defibrillation (continued)
– Ventricular fibrillation
 Thousands of electrical foci in heart depolarize
independently
 Myocardium quivers, cannot eject blood properly
– Ventricular Tachycardia
 Appears organized
 If patient is pulseless, treated the same a v-fib
– Never apply AED to patient with pulse.

– Does not restart heart.
– Electrical current passed through heart.
– Depolarizes cardiac electrical cells to stop them from
working independently of cardiac conduction system.
– Manual defibrillation requires training in recognition of
dysrhythmias; allows operator complete control over
timing and energy levels.

– AED analyzes cardiac rhythm; determines whether
pattern meets criteria for defibrillation; delivers shock.
– SAED analyzes rhythm in same way, but instead of
delivering shock, advises user shock is indicated.
– All AEDs require preventive maintenance to ensure
readiness.

Figure 17-22
Typical defibrillator pad placement.

– Check AEDs regularly.
– Replace batteries at specified intervals.
– Defibrillation pads expire; replace before expiration.
– AED applied only to patient in cardiac arrest;
unresponsive, apneic, pulseless.
– If AED available, apply and use quickly with little
interruption in chest compressions.

– Follow protocols to determine instances when
CPR started or continued prior to defibrillation.
– Defibrillator pads have adhesive and conductive
properties.
– Connect defibrillator pads to AED leads; apply to
patient’s bare chest.
 Make sure pad placed under breast tissue.
 Wipe chest dry before applying pads.

– Shave excessive chest hair before placing pads.
– Do not place pads over jewelry or medication patches.
– Do not place pads over internally implanted
pacemakers or defibrillators.
– AEDs preprogrammed to deliver shocks at given level.
– Newer AEDs and manual defibrillators deliver biphasic
energy; older models deliver monophasic energy.

– Attach pads to AED; apply to patient’s chest.
– Stop chest compressions.
– Clear personnel from patient to allow machine to
detect and analyze cardiac rhythm.

Scan 17-1 (1 of 6)
Initial Cardiac Arrest Management for Adult Patients
1. If a patient is apparently unresponsive and not breathing normally, check the carotid
pulse for no more than 10 seconds.

Scan 17-1 (2 of 6)
2. If you do not detect a carotid pulse in 10 seconds, begin chest compressions. A second
EMS provider should prepare to apply an AED while chest compressions are performed at
a ratio of 30 compressions to two ventilations.

Scan 17-1 (3 of 6)
3. Remove excess hair from the patient’s chest to ensure good contact between the
AED pads and the skin.

Scan 17-1 (4 of 6)
4. Apply the pads as directed by the manufacturer. The default position is to place the first
pad on the upper right chest, just below the clavicle and to the right of the sternal border.

Scan 17-1 (5 of 6)
5. The default position for the second pad is the lower left lateral chest.

Scan 17-1 (6 of 6)
6. When the defibrillator has been powered on (either before or after applying the pads,
according to the manufacturer’s directions), stop CPR, ensure that everyone is completely
clear of the patient, and press the designated button to analyze the rhythm (or allow the
AED to analyze the rhythm automatically, depending on the configuration). Allow the
machine to shock, or press to deliver a shock when prompted. Resume CPR.

– Fully automated defibrillator charges and delivers
shock once ventricular fibrillation or ventricular
tachycardia detected.
– Remain clear while machine delivers shock.
– As soon as shock is delivered, resume CPR even if
defibrillation is successful.

– After five cycles (two minutes), ending with
30 compressions, reanalyze rhythm.
– If shock advised, deliver as quickly as possible.
– If shock not advised, resume CPR.
– Monitor patient for signs of return of spontaneous
circulation (ROSC).

– Signs of ROSC:
 Resumption of spontaneous breathing
 Response to stimuli
 Detection of carotid pulse during pause in chest
compressions
– End-tidal carbon dioxide monitoring useful.

– Energy for defibrillation can be up to 360 Joules
for Monophasic monitor. Up to 200 Joules for
Biphasic monitor.
– If person in contact with patient, directly or indirectly,
electricity can be conducted to him or her.
– Always instruct all personnel to clear patient.

– Do not defibrillate in
 Moving ambulance
 Environment with combustible substance
 Wet conditions

• Intravenous access and medications
– CPR, defibrillation, establishing airway, providing
ventilations all take precedence over starting IVs and
administering medications.
– IVs established only when personnel present to allow
it without interrupting or delaying critical procedures.

• Resuscitation outcomes and
postresuscitation care
– Successful resuscitation
 Patient has ROSC; discharged from hospital
neurologically intact
– Most out-of-hospital attempts not successful

Figure 17-24 (1 of 2)
(A)
(A) Check the brachial pulse in infants.

Figure 17-24 (2 of 2)
(B)
(B) In two provider CPR, encircle the infant’s chest with your hands and place your thumbs
over the sternum to provide chest compressions.

Figure 17-25
Hand placement for child CPR.

• CPR in infants and children
– Pediatric cardiac arrest secondary from hypoxia
– Frequent cause is airway or breathing
 FBAO, asthma, respiratory infection, drowning, electrocution,
overdose, trauma
– Survival rates improved by bystander CPR
– Sequence begins with chest compressions.
– Lone rescuer compression ratio 30:2; two rescuers
ratio of 15:2;
– Likelihood asphyxial cardiac arrest.

• CPR in infants and children (continued)
– Compression rate 100–120 per minute.
– Infant
 under one year old.
– Children
 one year old until puberty

– Infants
 Check brachial pulse
 Two fingers placed over sternum or encircle chest with hands
and use thumbs to compress sternum
 Compress approx 1½ inches at 100–120 per minute
 Chest compressions used when heart rate is less than 60 per
minute with signs of poor perfusion

– Children
 Check carotid pulse
 Same CPR as for infants
 Use one or two hands (depending on size)
 Compress 2 inches

• Secondary assessment and history taking
in resuscitation
– Rapid intervention required for cardiac arrest.
– Rapid medical assessment.
– Obtain history.
– Know events that preceded cardiac arrest to identify
possible toxins, trauma, correctable conditions.

Table 17-7 (1 of 2)
Potentially Reversible Causes of Cardiac Arrest
Six Hs
Cause Factors and Actions
Hypoxia The most common cause of cardiac arrest in pediatric patients. Ensure an open
airway and adequate ventilations. Provide supplemental oxygen.
Hypovolemia Suspect with trauma or evidence of internal bleeding. Infuse IV fluids to
increase volume.
Hypoglycemia May be a cause of cardiac arrest in diabetic patients. Check blood glucose level
in all cardiac arrest patients and administer dextrose intravenously if indicated.
Hypothermia/hyperthermia Take note of the environment; suspect hypothermia in septic patients. Begin
passive rewarming for hypothermia; cool the patient with hyperthermia.
Hydrogen ion (acidosis) Occurs with hypoxia and ischemia. Ensure adequate ventilation, oxygenation,
and chest compressions.
Hypokalemia/hyperkalemia May occur in dialysis patients, diabetic patients, or patients with dehydration.
Obtain a good history of the present illness and past medical history.

Table 17-7 (2 of 2)
Potentially Reversible Causes of Cardiac Arrest
Five Ts
Cause Factors and Actions
Trauma Obtain a history from family or bystanders and perform a secondary assessment.
Toxins or tablets Includes overdoses, toxic exposure, and bites and stings. Perform a good scene size-
up, obtain a history from family and bystanders, perform a secondary assessment.
Thrombosis (stroke, ACS,
pulmonary embolism)
Obtain a history of the present illness and past medical history.
Tamponade (cardiac
tamponade)
Suspect with penetrating chest trauma or in medical conditions such as cancer.
Transport without delay.
Tension pneumothorax May occur from trauma or lung disease. Requires immediate decompression.
Transport without delay if paramedic assistance is not immediately available.

• Ethical and legal considerations
– Follow your protocols to determine when resuscitation
is and is not indicated.
– Do not initiate resuscitative efforts on patients
who have
 rigor mortis
 dependent lividity
 obvious decomposition
 injuries incompatible with life

• Ethical and legal considerations (continued)
– Terminally ill patients may have physician’s orders
for life-sustaining treatment (POLST).
 Follow protocols
– Look after well-being of bystanders and family
members.

• Return of spontaneous circulation
– Resuscitation of cardiac arrest frequently unsuccessful.
– If ROSC detected, continuously monitor patient for
subsequent deterioration and cardiac arrest.
– ROSC patients
 Rarely regain responsiveness
 Permanent neurological deficits common
 Manage airway and breathing; obtain vital signs; continuously
reassess patient

• Management of Body Temperature
– Patients with ROSC who remain comatose may
benefit from therapeutic temperature management
in hospital.
 32 to 36 degrees Celsius (89.6 to 96.8 Fahrenheit)
 Maintained for 24 hours

Chapter Summary (1 of 3)
• AEMTs must rapidly identify and treat patients in
shock and cardiac arrest to improve survival.
• Goal is to quickly restore tissue perfusion.
• In shock, priorities are to establish airway and
ensure patient is adequately ventilated and
oxygenated, and external bleeding controlled.

• In cardiac arrest, chest compressions highest
priority to reestablish circulation.
• Prompt defibrillation required for ventricular
fibrillation and pulseless ventricular tachycardia.
• Establish airway; providing ventilation is critical.
• Minimal interruption of chest compressions.

• In both cardiac arrest and shock, resuscitation
requires teamwork, communication, searching for
underlying cause.
• For all critically ill patients, apply clinical reasoning
to determine when additional interventions
required.
• To continue to provide patients with best
opportunity for survival, maintain awareness of
current research and changes in protocols.

Alexander ch17 lecture

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