Shock

BY
Anchal Gupta
M.ScNursing II year
KGMU,College of Nursing
SHOCK

INTRODUCTION
Shock is a serious life threatening condition
characterized by inadequate tissue oxygen perfusion,
which reduces the delivery of oxygen and other
essential nutrients to a level below that required for
normal cellular activities. Cellular injury and
destruction may occur and tissue and organ functions
deteriorate. 5/5/20202 SHOCK

DEFINITION
 Shock is defined as a condition in which systemic
blood pressure is inadequate to deliver oxygen
and nutrients to support vital organs and cellular
function.
(Mikhail, 1999).
 Shock is defined as life-threatening clinical
syndrome of cardiovascular collapse
characterized by an acute reduction of effective
circulating blood volume; and an inadequate
perfusion of cells and tissues. The end result is
hypotension and cellular hypoxia and may lead to
death
5/5/20203 SHOCK

INCIDENCE
 Hypovolemic is most common type
 Cardiogenic shock occurs in 5-10% in patients with
acute MI.
 Neurogenic shock is seen with all spinal cord injuries.
 In the Worcester Heart Attack Study, a community-
wide analysis, the reported incidence rate was 7.5%.
The literature contains few data on cardiogenic shock
in patients without ischemia.
Aug 6, 2019. 5/5/20204 SHOCK

STAGES OF SHOCK
 Initial Stage
 Compensatory Stage
 Progressive Stage
 Irreversible Stage
5/5/20205 SHOCK

INITIAL STAGE
 No overt clinical manifestation is seen in this
stage.
5/5/20206 SHOCK

COMPENSATORY STAGE
Pathophysiology
Regardless of cause of shock, body attempts to
compensate for a decrease in tissue perfusion in
a variety of ways.
Capillary hydrostatic pressure becomes lower than
colloidal osmotic pressure. Fluid moves from
interstitial space to intravascular space.
Reduction in mean arterial pressure inhibit
baroreceptor activity will lead to stimulation of
vasomotor center. 5/5/20207 SHOCK

Cont…..
Activation of sympathetic nervous system and release
of epinephrine & nor epinephrine
Stimulation of alpha-1 adrenergic receptors causes
selective vasoconstriction. Blood flow to heart & brain
is maintained. Blood flow to kidney, GI tract, lungs,
muscles & skin is decreased.
Beta adrenergic receptor stimulation causes a mild
increase in heart rate & force of contraction.
Sympathetic stimulation also causes dilatation of
coronary arteries resulting in an increase in O2 supply
to the myocardium. 5/5/20208 SHOCK

Renal hypoperfusion occur which lead to
increased renin release which lead to conversion
of angiotensinogen to Angiotensin-1 & to
Angiotensin-2 which stimulates adrenal cortex
which produces aldosterone. Aldosterone acts on
posterior pituitary gland Increased ADH secretion.
Increased reabsorption of water which increased
blood volume
5/5/20209 SHOCK

Clinical manifestation
 Altered sensorium-apprehension restlessness &
irritability caused by cerebral hypoxia.
 BP may be normal, reduced or elevated.
 Orthostatic hypotension is significant & indicates
absolute or relative volume depletion.
 A fall in the systolic pressure >15mm of Hg
when raised from a supine position to a elevation
of 90 degree or standing
 Heart rate is markedly increases and respiratory
rate is increased.
5/5/202010 SHOCK

Cont…..
 Urine output begins to decrease secondary to
renal hypo perfusion.
 Decreased saliva secretion secondary to
peripheral vasoconstriction which increases thirst.
 Vasoconstriction also results in cool & pale
extremities except in septic shock.
 The body temperature is slightly decreased
except in septic shock where it is elevated
 Bowel sounds hypoactive due to reduced
peristalsis.
5/5/202011 SHOCK

PROGRESSIVE STAGE
Compensatory mechanisms are becoming
ineffective to the patient. An aggressive
management is necessary to reverse the shock at
this stage.
5/5/202012 SHOCK

PATHOPHYSIOLOGY
When shock is not detected & the precipitating
cause is not corrected, during the earlier stages,
a massive sympathetic nervous system response
occurs.
Profound vasoconstriction occurs. Some of the
peripheral vessels become totally occluded.
Renal ischemia leads to further activation of RAAS
mechanism.
5/5/202013 SHOCK

Further vasoconstriction lead to fall in cardiac
output
Tissue hypoxia, anaerobic metabolism, lactic acid
accumulation occurs. Metabolic acidosis and
cardiac depression occur
5/5/202014 SHOCK

CLINICAL MANIFESTATION
 Deterioration in level of consciousness
 Diminished response to painful stimuli
 Hypotension, systolic is below 80 mm of hg
 Narrow pulse pressure
 Tachycardia is evident
 Deep shallow respiration
 Urine output decreases
5/5/202015 SHOCK

IRREVERSIBLE STAGE
 At this stage compensatory mechanisms have
failed which lead cellular necrosis. If timing
management is not done it progresses to multi
organ dysfunction. Death is imminent.
5/5/202016 SHOCK

PATHOPHYSIOLOGY
Sympathetic activity no longer compensates to
maintain homeostasis
Pooling of blood because of lack of vasomotor
tone, Thrombosis of small blood vessels occurs.
Continued tissue hypoxia resulting decreased
cardiac output & sustained vasoconstriction leads
to anaerobic metabolism & accumulation of lactic
acid.
5/5/202017 SHOCK

Accumulation of lactic acid & acid metabolites
leads to cellular death. Acidic environment
causes increased capillary permeability.
Fluid & plasma protein leaves the vascular space.
5/5/202018 SHOCK

 Unresponsive to stimuli
 Fall in systolic blood pressure and diastolic blood
pressure falls to zero
 Slower heart rate,weak pulse, pulse deficit may
present
 Cardiac dysrhythmias
 Hyperkalemia
 Shallow respiration
 Hypoxemia, respiratory acidosis
 Minimal urine output
 Skin is cold & clammy
 Cyanosis present
5/5/202019 SHOCK

TYPES OF SHOCK
 Hypovolemic shock
 Septic shock/ Vasogenic shock
 Cardiogenic shock
 Neurogenic shock
 Anaphylactic shock
5/5/202020 SHOCK

HYPOVOLEMIC
SHOCK
5/5/202021 SHOCK

Concept
 When the volume of blood is inadequate to fill
the intravascular space.( total reduction in the
intravascular volume).
5/5/202022 SHOCK

ETIOLOGY
 Hemorrhage
 Trauma to blood vessel & major bones
 Ruptured aneurysms
 Bleeding esophageal varices, Hemorrhoids, ulcers
 Diarrhea, vomiting
 Burns
5/5/202023 SHOCK

PATHOPHYSIOLOGY
Decreased circulating volume
Decreased venous return
Decreased preload
Decreased cardiac output
Decreased O2 supply
Impaired tissue perfusion
5/5/202024 SHOCK

5/5/202025 SHOCK

Cont…..
 Diaphoresis
 Cold clammy skin
 Cyanosis
 Decrease urine output
 Anxiety , agitation and confusion
 Increase pulse and respiration
5/5/202026 SHOCK

SEPTIC SHOCK
/VASOGENIC SHOCK
5/5/202027 SHOCK

Concept
 Massive peripheral vasodilatation causes shock
because the blood volume, although within
normal limits, is insufficient to fill the enlarged
vascular capacity. This leads to a decreased
venous return and a diminished cardiac output. It
includes septic shock.
5/5/202028 SHOCK

ETIOLOGY
 EXOGENOUS FACTORS
 Poisoning
 Insect bites
 Bee sting
 Scorpion bite
 Indwelling catheters,
 Manipulative Instrumentation
 Food allergies
 Drug toxicity
 ENDOGENOUS FACTORS
 Infection by Gram+ ve bacteria & Gram -ve bacteria
5/5/202029 SHOCK

PATHOPHYSIOLOGY
Invasion of microorganism
Release of endotoxin and this lead to release of
inflammatory mediators
Mediators causes vasodilatation and capillary
permeability
Massive dilation and Organ hypoperfusion
Decrease venous return and decrease end
diastolic volume
5/5/202030 SHOCK

Cont….
Decrease stroke volume lead to decrease cardiac
output
Decrease blood pressure, decrease tissue
perfusion
Multiple organ dysfunction occur
5/5/202031 SHOCK

 Increased heart rate
 Decreased Blood pressure
 Change in the sensorium
 Decreased urine output
 Elevated WBC count
5/5/202032 SHOCK

CARDIOGENIC
SHOCK
5/5/202033 SHOCK

Concept
 Cardiogenic shock is the failure of the heart to
pump blood adequately to meet the oxygenation
needs of the body. It occurs when the heart
muscle loses its contractile power. It most
commonly occurs in association with, and as a
direct result of, acute myocardial infaction (AMI).
It is the most common cause of death in the post
AMI patient (about 5 % to 10% of AMI patients
develop cardiogenic shock).
5/5/202034 SHOCK

ETIOLOGY
Deficient emptying
Myocardial infarction
Cardiomyopathies
Rupture of the heart, ventricle or papillary muscle
Cardiac arrhythmia
Deficient filling
Cardiac tamponade from haemopericardium
Obstruction to outflow
Pulmonary embolism
Tension pneumothorax
5/5/202035 SHOCK

Dissecting aortic aneurysm
 Impaired contractibility causes a marked
reduction in Cardiac output and ejection fraction.
 Decreased cardiac output results in lack of blood
and oxygen to the heart well as other vital organs
( brain and kidneys)
 Lack of blood and oxygen to the heart muscle
results in continued damage to the muscles, a
further decline in contractile power, and a
continued inability of the heart to provide blood
and oxygen to vital organs.
 MI causing extensive damage (40% or greater) to
the left ventricular myocardium is the most
common cause.
5/5/202036 SHOCK

PATHOPHYSIOLOGY
Primary ventricular ischemia
Structural problem
Dysarrhymias
Systolic dysfunction ineffective forward movement
of the blood
Decreased stroke volume Diastolic dysfunction
ineffective filling
Decrease cardiac output increase
pulmonary pressure 5/5/202037 SHOCK

Pulmonary oedema
Decreased oxygenation
Decreased tissue perfusion
Decreased cellular metabolism
5/5/202038 SHOCK

CLINICAL MANIFESTATIONS
 Confusion, restlessness, mental lethargy( due to
poor perfusion of brain)
 Low systolic blood pressure (90 mm Hg or 30 mm
Hg less than previous levels).
 Oliguria – urine output less than 30 ml/hour for at
least 2 hours (due to decreased perfusion of
kidneys).
 Cold, clammy skin (blood is shunted from the
peripheral circulation to perfuse vital organs);
profoundly diaphoretic with mottled extremities.
 Weak, thread peripheral pulses,fatigue,
hypotension ( due to inadequate CO).
5/5/202039 SHOCK

Cont…..
 Dyspnea, tachypnea, cyanosis ( increased left
ventricular pressures result in elevation of left
atrial and pulmonary pressures, causing
pulmonary congestion).
 Chest pain (due to lack of oxygen and blood to
heart muscle).
 Decreased bowel sounds (due to paralytic ileus
from decreased perfusion to GI tract.
 Metabolic acidosis due to increased lactate
production and reduced clearance ( caused by
anaerobic metabolism and liver dysfunction).
5/5/202040 SHOCK

Cont….
 Dysrhythmias (due to lack of oxygen to heart
muscle) and sinus tachycardia ( as a
compensatory mechanism for a decreased CO).
5/5/202041 SHOCK

NEUROGENIC SHOCK
5/5/202042 SHOCK

Concept
 Neurogenic shock is a distributive type of shock
resulting in low blood pressure, occasionally with
a slowed heart rate, that is attributed to the
disruption of the autonomic pathways within the
spinal cord. It can occur after damage to the
central nervous system, such as spinal cord injury
and traumatic brain injury.
5/5/202043 SHOCK

ETIOLOGY
 Spinal cord injury
 Spinal anesthesia
 Nervous system damage
 Depressant action of medication
5/5/202044 SHOCK

PATHOPHYSIOLOGY
Due to etiological factors (Spinal cord injury)
Loss of sympathetic tone
Venous and arterial vaso dilatation
Decrease venous return and end diastolic volume
Decrease stroke volume, cardiac output, blood pressure
Decreased tissue perfusion
Impaired cellular metabolism
5/5/202045 SHOCK

 Hypotension
 Bradycardia
 Hypothermia
 Dry skin
 Loss of motor function
 Loss of consciousness
5/5/202046 SHOCK

ANAPHYLACTIC SHOCK
5/5/202047 SHOCK

Concept
 Anaphylactic shock is the shock caused by a
severe allergic (immunologic) reaction when a
patient who has already produced antibodies to a
foreign substance (antigen) develops a systemic
antigen-antibody reaction and triggers abnormal
dilatation of blood vessels.
5/5/202048 SHOCK

ETIOLOGY
 Food such as legumes, shelfish, egg whites, milk,
chocolate, tomato and strawberries
 Stringes and bites of insect
 Snake venom
 Substances used to diagnose and treat the
diseases such as antibiotics , vaccine, iodine dye.
 Other substance such as pollen, latex
5/5/202049 SHOCK

PATHOPHYSIOLOGY
Due to etiological factors (Drugs/ bites)
Increase in allergic reaction
Antigen-antibody reaction
Release of histamine from mass cell/ basophil
Action of histamines leads to massive vasodilatations
5/5/202050 SHOCK

 Stridor, wheezing, respiratory distress
 Circulatory collapse
 Tachycardia
 Hypotension
 Vasodilatation
 Pruritis, erythema
5/5/202051 SHOCK

COMPLICATION
 Neurologic impairment
 ARDS
 Renal Failure
 Cardiopulmonary arrest
 Limb ischemia
 Death
5/5/202052 SHOCK

DIAGNOSTIC
EVALUATION
5/5/202053 SHOCK

 When a patient is suspected of having shock,
diagnostic evaluation should occur at the same
time as resuscitation.
 Resuscitative efforts should not be delayed for
history, physical examination, laboratory testing
imaging.
 Medical history and Physical examination
5/5/202054 SHOCK

 Laboratory evaluation-
 Altered hemodynamic parameters (pulmonary
artery wedge pressure 15 mm Hg or greater,
cardiac index [CI] less than 2.0, elevated
systemic vascular resistance[SVR], decreased
mixed venous oxygen saturation.
 Arterial blood gas
5/5/202055 SHOCK

 Chest X ray – pulmonary vascular congestion.
 Abnormal laboratory values- elevated blood urea
nitrogen, and creatinine, elevated liver enzyme,
increase PPT and PT, elevated serum lactate,
elevated brain natriuretic peptide.
 ECG- reveal myocardial injury
 Echocardiogram- valvular dysfunction
5/5/202056 SHOCK

MEDICAL
MANAGEMENT
5/5/202057 SHOCK

AIMS/GOALS
 Rapid diagnosis and prompt initiation of
pharmacologic therapy to maintain blood
pressure and cardiac output and respiratory
support.
 To treat underlying cause of shock.
 Any potential routes of infection must be
eliminated.
 Drainage of abscess and debridement of necrotic
areas.
5/5/202058 SHOCK

Cont……
 Proper antibiotic therapy based on culture and
sensitivity
 Recent studies have indicated that treatment for
cardiogenic shock from acute myocardial injury
should focus on revascularization and
thrombolytics.
 Augumenting cardiac output with devices (intra
aortic balloon pump) [IABP] is method of choice.
5/5/202059 SHOCK

EMERGENCY
MANAGEMENT
5/5/202060 SHOCK

Initial management
 Establish and maintain a patent airway
 Administer high flow oxygen (100%) by a non-
rebreather mask
 Anticipate need for intubation and mechanical
ventilation
 Stabilize cervical spine as appropriate
 Control external bleeding
 Draw blood for lab studies
 Establish 2 large bore catheters and begin fluid
resuscitation with crystalloids (normal saline)
 Antibiotic therapy
 Insert an indwelling bladder catheter and NG tube5/5/202061 SHOCK

Ongoing monitoring
 Level of consciousness
 Vital signs including pulse oximetry, peripheral
pulses and capillary refill
 Respiratory status
 Cardiac rhythm & cardiac output
 Urine output
5/5/202062 SHOCK

Fluid resuscitation
 Crystalloids
 Isotonic (0.9% NaCl, Ringer Lactate)
 Hypertonic (1.8%, 3%, 5% NaCl)
 Colloids
 Dextran 40
 Human Serum Albumin
 Blood and Blood products
 Whole blood / PRBC
 Fresh Frozen Plasma
5/5/202063 SHOCK

PHARMACOLOGIC THREAPY
 Positive inotropic drugs( epinephrine, dopamine,
dobutamine) stimulate cardiac contractibility,
dobutamine and amrinone may lower BP.
 VASODILATOR THERAPY – decrease the
workload of the heart by reducing venous return
and lessening resistance against which the heart
pumps (preload and after load reduction). Cardiac
output improves left ventricular pressures and
pulmonary congestion decreases and myocardial
oxygen consumption is reduced. Example –
dopamine & dobutamine and Oxygen
5/5/202064 SHOCK

Cont….
 VASOPRESSOR THERAPY – may be needed to
maintain adequate perfusion pressure
 ( MAP 70 mm hg or greater) Example – dopamine
& adrenaline.
 DIURETIC THERAPY – decreases total body
fluid volume and relieves systemic and pulmonary
congestion. Example- Nesiritide may be
considered for treatment with heart failure.
5/5/202065 SHOCK

OTHER MEDICAL THERAPY
 COUNTERPULSATION THERAPY- Improves
blood flow on the heart muscle and reduces
myocardial oxygen needs. Results in improved
cardiac output ( 1.5 l/min increases) and
preservation of viable heart tissue.
 LEFT VENTRICULAR ASSIST DEVICE- Device
used to unload the left ventricle as bridge to
recovery, transplant or destination. May only be
performed in areas where immediate access to
emergency cardiac surgery is available. 5/5/202066 SHOCK

NURSING CARE PLAN
5/5/202067 SHOCK

Nursing assessment
Clinical assessment begins with attention to the airway/breathing/
circulation and vital signs.
1.Identify patients at risk for development of cardiogenic shock.
2.Assess for early signs and symptoms indicative of shock:
 Restlessness, confusion, or change in mental status.
 Increasing heart rate
 Decreasing pulse pressure
 Decrease urine output, weakness and fatigue
5/5/2020SHOCK68

Cont…..
3.Observe for presence of central and peripheral cyanosis
4.Observe for development of edema
5.Identify patient’s and significant other’s reaction to crisis
situation.
5/5/2020SHOCK69

1. Impaired gas exchange related to change in the alveolar capillary membrane as
evidenced by abnormal arterial blood gas analysis
NURSING INTERVENTION RATIONALE
1.Assess the client’s respiratory rate,
rhythm, and depth.
1.During the early stages of shock, the
client’s respiratory rate will be
increased due to hypercapnia and
hypoxia. Once the shock progresses,
the respirations become shallow, and
the client will begin to hypoventilate.
2.Assess client heart rate and blood
pressure
2.The client’s blood pressure and heart
rate will decrease and
dysrhythmias may occur
3. Monitor oxygen saturation using
pulse oximetry
Pulse oximetry is used in measuring
oxygenation concentration. The
normal oxygen saturation should be
maintained at 90% or higher
5/5/2020SHOCK70

Cont…..
4. Monitor arterial blood gasses.
5. Assist the client when coughing,
and suction the client when needed.
4. Increasing PaC02 and decreasing
Pa02 are signs of hypoxemia and
respiratory acidosis.
5. Suction removes secretions if the
client is unable to effectively clear
the airway.
5/5/2020SHOCK71
EXPECTED EVALUATION – Client will maintain optimal gas exchange, as
evidenced by ABGs within the normal range, oxygen saturation of 90% or
greater.

2. Decreased cardiac output related to impaired left ventricular contractibility as
evidenced by changes in the level of consciousness
1.Assess for any changes in the level of
consciousness.
1. Restlessness and anxiety are early
signs of cerebral hypoxia
while confusion and loss of
consciousness occur in the later stages.
2. Assess the central and peripheral
pulses.
2. Pulses are weak, with
diminished stroke volume and cardiac
output.
3. Monitor the client’s central venous
pressure (CVP), pulmonary artery
diastolic pressure (PADP), pulmonary
capillary wedge pressure, and cardiac
output/cardiac index.
3.CVP provides information on filling
pressures of the right side of the heart;
pulmonary artery diastolic pressure and
pulmonary capillary wedge pressure
reflect left-sided fluid volumes. Cardiac
output provides an objective number to
guide therapy.
5/5/2020SHOCK72

Cont…
4. Provide electrolyte replacement as
prescribed.
4.Electrolyte imbalance may
cause dysrhythmias or other
pathological states.
5. Restrict fluids and sodium as
ordered if increased preload becomes
a problem.
5. Fluid resuscitation
reduces extracellular fluid volume
and decreases cardiac workload
5/5/2020SHOCK73
EXPECTED EVALUATION – Client will maintain adequate cardiac output
as evidenced by strong peripheral pulses, HR 60-100 beats per minute with
regular rhythm.

3. Ineffective tissue perfusion related to cessation of blood flow as evidenced by
abnormal arterial blood gas analysis
1. Assess the client’s HR, BP, and
pulse pressure
1. Sinus tachycardia and increased
arterial BP are seen in the early
stages to maintain an adequate
cardiac output. BP drops as condition
deteriorates
2. Monitor oxygen saturation and
arterial blood gasses.
2. Pulse oximetry is used in
measuring oxygenation
concentration. The normal oxygen
saturation should be maintained at
90% or higher
3. Restrict the patient’s activity, and
maintain the client on a bed rest
3. Minimize oxygen demand by
maintaining bed rest and limiting the
client’s activity
5/5/2020SHOCK74

Cont….
4. Provide oxygen therapy as
indicated
4. Oxygen is administered to
increase the amount of oxygen
carried by available hemoglobin in
the blood
5/5/2020SHOCK75
EXPECTED EVALUATION – Client will demonstrate increased perfusion
as individually appropriate as evidenced by strong peripheral pulses, HR
60-100 beats per minute with regular rhythm, systolic B.P within 20 mm hg
of systolic.

4. Excess fluid volume related to increase sodium and water retention as
evidenced by edema
1. Monitor urine output, observe its
color and amount.
1.Urine output may be concentrated
and scanty due to decreased renal
perfusion
2. Monitor client’s intake and output 2. Decreased cardiac output may lead
to decreased renal perfusion and
impairment with excess fluid volume
which causes water and sodium
retention and oliguria
3. Assess for edema 3. Edema (usually pitting edema)
that starts in the feet and ankles and
gradually lead to weight gain
5/5/2020SHOCK76

Cont…
4. Assess fluid balance and weight
gain
4. Fluid and sodium retention occurs
due to the compromised regulatory
mechanisms. Body weight is used to
detect response to diuretic therapy
5. Place the client in a semi position
6. Administer diuretics
(e.g.furosemide) as indicated
5. Semi flower position increases
renal filtration and decreases the
production of ADH thus promoting
diuresis.
6. Diuretics decrease plasma volume
and peripheral edema
5/5/2020SHOCK77
EXPECTED EVALUATION – Client will have stable fluid volume as
evidenced by balance intake output, stable weight , vital signs within
normal limits and absence of edema.

5. Anxiety related to fear of death as evidenced by avoid looking at equipment or
keeps vigilant watch over equipment
1. Assess previous coping
mechanism used
1. . Anxiety and ways of decreasing
perceived anxiety are highly
individualized. Interventions are
most effective when they are
consistent with the client’s
established coping pattern
2. Explain all procedures as
appropriate, keeping explanations
basic
2. Information helps reduce anxiety.
Anxious clients unable to understand
anything more than simple, clear,
brief instructions
3. Encourage the client to verbalized
his or her feelings
3. Talking about anxiety-producing
situations and anxious feelings can
help the client perceive the situation
in a less threatening manner
5/5/2020SHOCK78

CONT….
4. Maintain a confident, assured
manner while interacting with the
client. Assure the client and
significant others of close,
continuous monitoring that will
ensure prompt intervention
4. The staff’s anxiety may be easily
perceived by the client. The client’s
feeling of stability increases in a
calm and non-threatening
atmosphere. The presence of a
trusted person may help the client
feel less threatened
5/5/2020SHOCK79
EXPECTED EVALUATION – Client will describe reduction in level of
anxiety experienced.

Patient education and health maintains
 Assess patient readiness to learn.
 Teach patients taking digoxin the importance of taking their
medication as prescribed, taking pulse before daily dose and
reporting for periodic blood levels.
 Teach sign of impending heart failure- increasing edema ,
shortness of breath ,decreasing urine output and increasing pulse.
5/5/2020SHOCK80

Cont….
 Have low sodium, low fat diet and reiterate the importance of
adhering to this diet.
 Explain to the patient the need to work with a physical and
occupational therapist – especially for low ejection fraction – for
energy conservation.
5/5/2020SHOCK81

Related research
Implementation of a Cardiogenic Shock Team and Clinical Outcomes
(INOVA-SHOCK Registry): Observational and Retrospective Study.
5/5/2020SHOCK82

Objective
(1) to collect retrospective clinical outcomes for acute decompensated heart
failure cardiogenic shock and acute myocardial infarction cardiogenic
shock, and compare current versus historical survival rates and clinical
outcomes;
(2) to evaluate Inova Heart and Vascular Institute site specific outcomes
before and after initiation of the Cardiogenic Shock team.
(3) to compare outcomes related to early implementation of mechanical
circulatory support and hemodynamic-guided management versus
historical controls;
(4) to assess survival to discharge rate in patients receiving intervention from
the designated shock team
5/5/2020SHOCK83

 The preliminary results of this study demonstrate
that the INOVA SHOCK team approach to the
treatment of Cardiogenic Shock with early team
activation, rapid initiation of mechanical
circulatory support, hemodynamic-guided
management, and strict protocol adherence is
associated with superior clinical outcomes:
survival to discharge and overall survival when
compared to 2015 and 2016 outcomes prior to
Shock team initiation.
5/5/202084 SHOCK

References
 Sathya P, Devanand viji ,’Textbook of
Physiology’,3rd edition(2013),published byCBS
Publishers & distributors .page no. 156 -163.
 Sharma K. Suresh ‘Manual of Medical Surgical
Nursing ‘,2th edition (2017),published by Wolters
Kluwer.
 Chintamani ,’Lewis ‘s Medical Surgical Nursing
‘,1st edition (2011),published by Elsevier. Page
no. 48-94
5/5/202085 SHOCK

 Woods L. Susan, “Cardiac Nursing”, 6 th edition
(2009), published by Wolters Kluwer. Page no.56-
58.
 Tehrani Behman, Alexander Trusedell,etal. :-
Implementation of a Cardiogenic Shock Team and
Clinical Outcomes (INOVA-SHOCK Registry):
Observational and Retrospective Study.2018 Jan;
7(6). Avialable from:-
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC60
43735/
 https:// emedicine.medscape.co
5/5/202086 SHOCK

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