shock - ncm 106
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7/29/2019 SHOCK - NCM 106
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By: Yamon, Abigail Faye A.
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Circulatory System Review
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Adequate blood flow to the tissues
and cells requires the following:
Adequate cardiac pump
Effective vasculature or circulatory system
Sufficient blood volume
If one component is impaired, perfusion to the tissues is
threatened or compromised.
Without treatment, inadequate blood flow to the tissues
results in poor delivery of oxygen and nutrients to the cells,
cellular starvation, cell death, organ dysfunction
progressing to organ failure and eventual death
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The cell swells & the cell membrane becomes more permeable; fluids & electrolytes seep from
& into the cell. Mitochondria & lysosomes are damaged & the cell dies
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Nutrients
Metabolically broken down
Stored in a form of
Adenosine Triphosphate (ATP)
Stored in Mitochondria
Transports substances
(Sodium, Potassium,Calcium) through the
cell membrane
Synthesize chemical
compounds
(cholesterol & protein)
Supplies energy for
mechanical work like
muscle contraction
Energy metabolism
within the cell
Mitochondria - cell's power producers, they convert
energy into forms that are usable by the cell.
Normal Cellular Function
Specialized cellular
function, conductionof electrical impulses
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ATP production
slows down
Lactic acid goes through the bloodstream and the muscles
Body attempts to produce ATP to fuel the cells
Build up of lactic acid
Accumulation of the toxic end product, lactic acid
Anaerobically metabolism
(in the absence of oxygen)
Lactic acid diffuses out of the cell membrane
Cell’s response to nerve
stimulation is inhibited
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CARDIAC CYCLE
Systole100 – 120 mmHg
Diastole60 – 80 mmHg
Relaxation & filling of
the atria & ventricles
Contraction &
emptying of the atria
& ventricles
Systolic BP – Diastolic BP = Pulse Pressure
120 mmHg – 80 mmHg = 40 mmHg
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70mls X 70bpm =
4,900 mls or
approximately 5L
Approx. 5L/min.
(average)
- volume of blood
ejected from the
left ventricle intothe aorta per
minute
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StrokeVolume
Determined by 3 factors:
- the amt. of blood ejected by the
left ventricle into the aorta per
beat (60-100ml/beat)
Contractility
-refers to the force of
contraction, it is
related to the number
and status of myocardial cells.
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MAP = Systolic BP + 2 (diastolic BP)
3
Mean Arterial BP = CO X Peripheral Resistance(Peripheral Resistance is determined by the diameter of arterioles)
Normal Range: 70 – 105 mm Hg
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Definition
SHOCK
A condition in which tissue
perfusion is inadequate to deliveroxygen and nutrients to support
vital organs and cellular function
(Hameed, Aird, & Cohn, 2003).
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TYPES OF SHOCK
Hypovolemic Occurs when there is a decrease
in the intravascular volumeCardiogenic Occurs when the heart has an
impaired pumping ability
Distributive:
Anaphylactic Caused by hypersensitivity
reactionSeptic Caused by an infection
Neurogenic Caused by alterations in
vascular smooth muscle tone
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Initiating
stimulus
( BP)
Symphatetic
stimulation
RAAS
Activation
Unresolved process
Failure of
Compensatory
Mechanisms
Cellular hypoxia, anaerobic
metabolism, lactic acidosis
Myocardial
contractility &
bradycardia
SVR
Peripheral
vasodilation
Permeability
capillary bed
& pooling
CO
Irreversible tissue
& organ damage
Failure of organs &
systems of body
DeathHR, SVR
Compensated
Shock
Decompensated
Shock
Irreversible
Shock
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Decrease in cardiac output & tissue perfusion
Sympathetic nervous system activation
Renin-
angiotensin
activation
Vascular compliance, blood volume, & cardiac output
Restoration of tissue perfusion
Initial physiologic insult leading to shock state
Endocrine response
Vasoconstriction & activation of
ADH Preload
Blood pressure,
heart rate &
myocardial
contractilityRenal system conserves
Na & H2O Preload
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CO
Fluid moves from
tissues into vascular
system
Hydrostatic pressure
w/in capillaries
Compensatory Stage
Circulating volume
Sympathetic stimulation
Epinephrine &
norepinephrine released
Vasoconstriction
Systemic vascularresistance
BP maintained
Tachycardia
Capillary blood flow
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SVR
Systemic BP
Vascular tension
Reduced tension in afferent arteriole of kidneys
JG cells release renin
Stretch receptors in JG cells of kidneys respond to volume & pressure
Renin acts to split angiotensinogen (a protein release by liver)
Generation of angiotensin I
Converts to angiotensin II (vasoactive peptide)
Stimulates zona glomerulosa of adrenal
cortex to form & release aldosterone
Aldosterone causes Na+ & H20
reabsorption by the kidneys Restoration of blood volume Increased BP
Converted in
some tissues to
angiotensin III
Arteriolar diameter
(vasoconstriction)
Converting
enzyme from lung
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Clinical Manifestations
• Increased respiratory rate – in response tometabolic acidosis
• Increased pH
•
Compensatory respiratory alkalosis• Change mental status (confusion or
combativeness) – alkalotic state
• Arteriolar dilation
If treatment begins in this stage of shock, theprognosis for the patient is good.
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Medical Management
• Directed toward identifying the cause of the
shock
• Correct the underlying disorder so that shock
does not progress
• Support physiologic process
• Fluid replacement & medication therapy to
maintain adequate BP & reestablish, &
maintain adequate tissue perfusion
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Management
• Directed toward identifying the cause of the
shock, correcting the underlying disorder so
that shock does not progress, and supporting
those physiologic processes that thus far haveresponded successfully to the threat.
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Nursing Management
• Monitor tissue perfusion
- Monitor hemodynamic status & promptly
report deviations to the physician
- Report a systolic BP lower than 90mmHg
or a drop of 40mmHg
- Administer prescribed fluids &
medications and promote patient’s safety,
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Nursing Management
• Several new technologies to detect changes in
tissue perfusion before changes in classic signs
(BP, HR, UO) indicate hypoperfusion
-SUBLINGUAL CARBON DIOXIDE
-GASTRIC TONOMETRY
-CENTRAL VENOUS or MIXED VENOUS BLOOD
OXYGEN SATURATION (SvO2)
-CAPNOGRAPHY
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Nursing Management
• Reducing Anxiety
– Provide brief explanations about the diagnostic
and treatment procedures
– Support the patient during diagnostic procedures,
and provide information about the outcomes of
diagnostic procedures
–
Speak in calm manner, reassuring voice & usinggentle touch
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Nursing Management
• Promoting Safety
- Monitor potential threats to the patient’s
safety because a high anxiety level & altered
mental status typically impair judgment
- Close monitoring & frequent reorientation
because patient may disrupt IV lines &
catheters that may complicate their condition
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Recognizing early signs of shock in
older patients•
Medications such as beta-blocking agents (metoprolol[Lopressor]) may mask tachycardia a primary compensatory
mechanism to increase CO during hypovolemic states.
• Aging immune system may not mount a truly febrile response,
but an increasing trend in body temperature should beaddressed.
• The heart does not function well in hypoxemic states & the
aging heart may respond to decreased myocardial
oxygenation with dysrhthmias that may be misinterpreted as
normal part of the aging process
• Changes in mentation may be inappropriately misinterpreted
as dementia. Older people with a sudden change in mentation
should be aggressively treated for the presence of infection &
organ hypoperfusion.
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Progressive Stage
• Mechanisms that regulate BP can no longer
compensate
• MAP falls below normal limits
• Hypotensive (systolic BP <90 mm Hg)
• Prognosis worsens
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Progressive Stage
• Overworked heart dysfunctional
• Body’s inability to meet increased O2 requirements ischemia
• Biochemical mediatorsmyocardial depression failure of cardiac pump (even if the underlying cause of shock is not of cardiac origin)
• Autoregulatory function of the microcirculation fails inresponse to the numerous biochemical cytokines &mediators released by the cells increased capillarypermeability with areas of arteriolar & venousconstriction compromising cellular perfusion
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Progressive Stage
• Relaxation of precapillary sphincters causes fluidto leak from the capillaries interstitial edema& return of less fluid to the heart
•
Inflammatory response to injury is activated &proinflammatory & antiinflammatory cytokinesmediators are released activate coagulationsystem in an effort to reestablish homeostasis
• Body mobilizes energy stores & increases oxygenconsumption to meet increased metabolic needsof underperfused tissues & cells
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Progressive Stage
• Chances of survival depend on the patient’s
general health before the shock state as well
as the amount of time it takes to restore tissue
perfusion.
• Organ systems decompensates (respiratory,
cardiovascular, neurologic, renal, hepatic, GI,
hematologic)
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Medical Management
• Optimize intravascular volume
• Support the pumping action of the heart
• Improve the competence of the vascular system
•
Support the respiratory systemOther aspects:
• Early enteral nutritional support
• Aggressive hyperglycemic control with IV insulin
• Antacids, histamine – 2 (H2) blockers, orantipeptic agents reduce the risk of GIulcerations & bleeding
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Nursing Management
• Prevent complications
• Promote rest & comfort
• Support family members
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Irreversible Stage
• “refractory stage”
• Does not respond to treatment & cannot survive
• Despite treatment BP remains low
•
Renal & liver failure compounded by the release of necrotic tissue toxins overwhelming metabolicacidosis
• Anaerobic metabolism contributes to a worsening
lactic acidosis• Reserves of ATP almost totally depleted & mechanisms
for storing new supplies of energy have been destroyed
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Irreversible Stage
• Respiratory system failure prevents adequate
oxygenation & ventilation despite mechanical
ventilatory support
• Cardiovascular system is ineffective in
maintaining MAP for tissue perfusion
• MODS complete organ failure death
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Medical Management
• Same as for the progressive stage
• Antibiotic agents & immunomodulation
therapy may be tried to reduce or reverse the
severity of shock
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Medical Management
• Depends on the type of shock & its underlying cause• Medications that are common to all types of shock:
- optimize intravascular volume
-support the pumping action of the heart
-improve the competence of the vascular system
-support the respiratory system
Other aspects of management:
-early enteral nutritional support
-aggressive hyperglycemic control with IV insulin
-antacids, histamine – 2 (H2) blockers, antipeptic agentsto reduce the risk of GI ulcerations & bleeding
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Nursing Management
• Preventing complications
• Promoting rest & comfort
• Supporting family members
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Finding COMPENSATORY PROGRESSIVE IRREVERSIBLE
BP Normal Systolic <80-90mmHG
Requires mechanical orpharmacologic support
HR >100bpm >150bpm Erratic or asystole
Respiratory
Status
>20 breaths/min Rapid, shallow
respirations;
crackles
Requires intubation
Skin Cold, clammy Mottled, petechiae Jaundice
Urinary output Decreased 0.5mL/kg/hr Anuric, requires
dialysis
Mentation Confusion Lethargy Unconscious
Acid-base
balance
Respiratory
alkalosis
Metabolic acidosis Profound acidosis
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SIGNS AND SYMPTOMS
Early Stage
(SNS
activation)
Restlessness , confusion
Tachycardia
TacypneaDiaphoresis; cold clammy skin
Decrease body temperature
Decrease urine output
Thirst, dry mucous membraneHypokalemia
Respiratory alkalosis (due to tachypnea, there is loss of
carbon dioxide)
Late Stage Hypotension, oliguria anuriaShallow respiration
Hypothermia
Decreased bowel sounds
Hyperkalemia, respiratory & metabollic acidosis
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Diagnostic Assessment
• Spirometry, pulse oximeter – respiratory status• ABG analysis – to determine whether the metabolic
acidosis that occurs with shock is being effectivelycombated by hyperventilation
• CVP - to estimate fluid loss• Pulmonary artery or Swan-Ganz catheter – to assist
with assessments of fluid status, cardiac function, &tissue oxygen consumption
•
Monitoring tools: cardiac monitor & the 12-lead ECG• Laboratory studies: CBC, blood chemistry, blood and
body fluid cultures
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• CVP- Pressure within the superior vena cava, or a
balloon flotation catheter in the PA
- Normal CVP Pressure: 2 – 12 mm Hg
- Decreased CVP decrease circulating volume
- Client should be relaxed (straining, coughing orany other activity that increases intrathoracic
pressure can cause falsely high measurements)- If with ventilator – readings at the point of endexpiration for greatest accuracy
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Assessing CVP Readings
ToAssess
Increased CVP(>11cm H2O)
Decreased CVP(<3cm H2O )
Blood
Volume
Increased
circulatingvolume
Decreased
circulatingvolume
Vascular
Tone
Vasoconstriction
HPN
Vasodilation,
peripheral
pooling
Septic Shock
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• Pulmonary Artery or Swan-Ganz catheter
- Via percutaneous puncture of the brachial,
subclavian, jugular, or femoral vein using
sterile technique
- Catheter is connected to a transducer & a
fluid-filled pressure monitoring system
- Potential complications: PA infarction, PE,
injury to the heart valves and myocardium
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Potential
complications:
PA infarction, PE,injury to the
heart valves &
myocardium
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Nursing Diagnosis
• Ineffective Tissue Perfusion
Other potential nursing diagnosis:
• Decreased Cardiac Output
• Risk for Impaired Gas Exchange
• Deficient Fluid Volume
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TYPES OF SHOCK
• Hypovolemic Shock
a. Hemorrhagicb. Dehydration
c. Burn
• Cardiogenic Shock
a. Excessive preload
b. Reduced preload
c. Excessive afterload
• Distributive Shock
a. Neurogenic (Vasogenic)
b. Septic Shock
c. Anaphylactic/Anaphylactoid
HYPOVOLEMIC SHOCK
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HYPOVOLEMIC SHOCK
Due to inadequate circulating blood volume resulting from:
*Hemorrhagic Results from a significant loss of whole bloodfrom trauma, GI bleeding, coagulation defects
*Dehydration Results from an extensive loss of body fluid
that depletes tissue fluid
*Burn Results from loss of plasma proteins, which
alters colloid osmotic pressure & leads to
edema. Chemical mediators in tissues enhance
fluid exudation to tissues. Central blood
volume is markedly depleted
The most common type of shock and develops when the intravascular
volume decreases to the point where compensatory mechanisms are
unable to maintain organ & tissue perfusion
CAUSES/Ri k F t
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CAUSES/Risk Factors:
EXTERNAL FLUID
LOSSES
INTERNAL FLUID
SHIFTS
Trauma
SurgeryVomiting
DiarrheaDiuresis
Diabetes Insipidus
Hemorrhage
BurnsAscites
PeritonitisDehydration
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Pathophysiology of HypovolemiaDecreased intravascular volume
Decreased CO
SNS stimulationInterstitial fluid
shiftsintravascularly vasoconstriction Increased HR
Increased renin,
aldosterone, ADH
Volume retention
Increased BP, blood volume
Continued loss of volume
Failure of compensatory mechanisms
Cellular hypoxia
Anaerobic metabolismImpaired cellular metabolism Irreversible changes
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Management of HYPOVOLEMIC SHOCK
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Management of HYPOVOLEMIC SHOCKEtiology Clinical Situation Intervention
Blood loss Massive trauma
GI bleeding
Ruptured aortic
aneurysm
Surgery
Erosion of vesselfrom lesion, tubes,
or other devices
Stop external bleeding with direct
pressure, pressure dressing,
tourniquet (as last resort)
Reduce intra-abdominal or
retroperitoneal bleeding by applying
MAST garment or prepare foremergency surgery
Administer Lactated Ringer’s or NS
(isotonic)
Transfuse with fresh whole blood,
packed cells, fresh frozen plasma, or
other clotting factors (if significant
improvement does not occur with
crystalloid administration)
Management of HYPOVOLEMIC SHOCK
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Management of HYPOVOLEMIC SHOCKEtiology Clinical Situation Intervention
Blood loss Massive trauma
GI bleedingRuptured aortic
aneurysm
Surgery
Erosion of vessel fromlesion, tubes, or other
devices
Use non-blood plasma expanders
(albumin, hetastarch, dextran) untilblood is available
Conduct autotransfusion if
appropriate
Plasma
loss
Burns
Accumulation of intra-abdominal fluid
Malnutrition
Severe dermatitis
DIC
Administer low-dose cardiotonics
(dopamine: dose range 5-20mcg/kg/min; begin infusion at
5mcg/kg/min; increase infusion
rate according to BP & other
clinical responses; dobutamine:
usual dose is 2-20mcg/kg/min IV)
Management of HYPOVOLEMIC SHOCK
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Management of HYPOVOLEMIC SHOCKEtiology Clinical Situation Intervention
Crystalloid
loss
Dehydration (ex. DKA,
heat exhaustion,protracted vomiting,
diarrhea, nasogastric
suction)
Administer isotonic or hypotonic
saline with electrolytes as neededto maintain normal circulating
volume & electrolyte balance
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• Trendelenburg position
Etymology: Friedrich Trendelenburg
• a position in which the head is low and the
body and legs are on an inclined plane. It issometimes used in pelvic surgery to displacethe abdominal organs upward, out of thepelvis, or to increase the blood flow to thebrain in hypotension and shock.
Mosby's Medical Dictionary, 8th edition. © 2009, Elsevier.
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Modified Trendelenburg - the lower extremities are elevated to
an angle of about 20 degrees; the knees are straight, the trunk is
horizontal & the head is slightly elevated.
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- Modified trendelenburg is the desired
position of the client during shock. The patient
is placed in supine position with the legs
elevated at 20-30 degree angle, the hipsslightly higher than the torso. To increase
venous return to the heart & to strengthen
contractility of the heart. Provide head pillowsupport to prevent cerebral venous
congestion & an increase ICP
CARDIOGENIC SHOCK
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CARDIOGENIC SHOCKDue to inadequate pumping action of the heart because of
primary cardiac muscle dysfunction or mechanical
obstruction of blood flow caused by:
*Excessive preload
-Acute MI,
Myocarditirs,mitral/aortic valvular
insufficiency,
ventricular septal
defects, congenital
conditions causingright heart failure, COPD
Poor cardiac contractility leads to increased
end-diastolic pressure and decreased BP. SNS is
activated to increase afterload; renin-angiotensin increases preload (aldosterone) and
after load (angiotensin II). Heart unable to
pump under increased stress. CO decreases, BP
decreases, tissue perfusion declines & acidosis
impairs cardiac functioning further.
Occurs in 10 % - 15% of all clients after MI & carries associated
mortality rate of up to 80%. Cardiogenic shock after MI usually occurs
when 40% or more of the myocardium has been damaged.
CARDIOGENIC SHOCK
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CARDIOGENIC SHOCK*Reduced
Preload-Pericardial
tamponade, RVI,
tension
pneumothorax
Restriction of input to the heart occurs
with tamponade and tensionpneumothorax. RVI causes decreased
blood flow to left ventricle due to poor
contractility. Standard SNS responses occur,
but increased HR does not compensate forfilling defect.
*Excessive
afterload
- Massivepulmonary
embolism, systemic
hypertension,
aortic stenosis
Gradual onset of heart failure and shock occurs
when heart cannot maintain the pressures
required from hypertension & aortic stenosis, thehypertrophied left ventricle decompensates, heart
failure ensues, BP declines. In massive PE, sudden
right heart failure develops from obstruction to
flow
Causes/Risk Factors:
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Causes/Risk Factors:
Excessive preload
-Acute MI,Myocarditirs,
mitral/aortic
valvular
insufficiency,
ventricular septal
defects, congenital
conditions causingright heart failure,
COPD
Reduced
Preload-Pericardial
tamponade,
RVI, tension
pneumothorax
Excessive
afterload- Massive
pulmonary
embolism,
systemic
hypertension,
aortic stenosis
Pathophysiology of Cardiogenic Shock
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Pathophysiology of Cardiogenic Shock
Renin, aldosterone, ADH,
catecholamine release
Pulmonary
or systemiccongestion
Decrease CO
Decreased coronary
artery perfusion
Decreased O2 &
nutrients available
to tissues & organs
Compensatory response
Increased blood
volume, SVR
Increased HR, stroke volume, & preload
Inability toovercome
increase
afterload
Increasedmyocardial
oxygen
demands
Decrease BP
Decreased
further
contractility
Impaired cellular
metabolism
Anaerobic
metabolism
Lactic acidosis&
depressed organ
function
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Management of CARDIOGENIC SHOCK
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Management of CARDIOGENIC SHOCKEtiology Clinical Situation Intervention
Myocardial
disease orinjury
Acute MI,
Myocardialcontusion
Cardiomyopathies
Fluid-challenge with up to 300ml of
NSS or Ringer’s lactate to rule outhypovolemia, unless HF or PE is present
Monitor CO, pulmonary artery
pressure & PCWP; administer IVF to
maintain left ventricular filling pressureof 15-20mmHg
Administer inotropics (dopamine or
dobutamine)
Vasodilators , diuretics, cardiotonics,
betablockers, glucocorticosteroids
Intra-aortic balloon pump or external
counterpulsation device if
unresponsive to other therapies
Management of CARDIOGENIC SHOCK
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Management of CARDIOGENIC SHOCKEtiology Clinical Situation Intervention
Valvular
disease orinjury
Ruptured aortic
cusp (sudden heart
failure)
Ruptured capillary
muscle
Thrombus
Fluid-challenge with up to 300ml of NSS or
Ringer’s lactate to rule out hypovolemia, unlessHF or PE is present
Monitor CO, pulmonary artery pressure &
PCWP; administer IVF to maintain left
ventricular filling pressure of 15-20mmHg
Administer inotropics (dopamine ordobutamine)
Vasodilators , diuretics, cardiotonics,
betablockers, glucocorticosteroids
Intra-aortic balloon pump or external
counterpulsation device if unresponsive to
other therapies
If rapid response does not occur, prepare for
prompt cardiac surgery
Management of CARDIOGENIC SHOCK
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Management of CARDIOGENIC SHOCKEtiology Clinical Situation Intervention
External
pressure onthe heart
interferes
with heart
filling oremptying
Pericardial
tamponade due totrauma, aneurysm,
cardiac surgery,
pericarditis
Massive pulmonaryembolus
Tension
pneumothorax
Ascites
Relieve tamponade with ECG-assisted
pericardiocentesis; repair surgically if itrecurs
Thrombolytic (streptokinase) or
anticoagulant (heparin) therapy; surgery
for removal of clot (embolectomy)
Relieve air accumulation with needlethoracostomy or chest tube insertion
Relieve fluid accumulation with
paracentesis
Cardiac
dysrhythmias
Tachydysrhythmias
Bradydysrhythmias
Pulseless electrical
activity
Treat dysrhthmias; be prepared
to initiate CPR, cardiac pacing
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Needle Thoracostomy
DISTRIBUTIVE SHOCK
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DISTRIBUTIVE SHOCKAlso called “VASOGENIC SHOCK”
Due to changes in blood vessel tone that increase inthe circulating blood volume.
*Neurogenic Shock
(Vasogenic)
- CNS damage tovasomotor center,
cerebral edema,
general anesthetic
medullary
depression,
cervical, spinal cord
injury
Interference with nervous system
control of the blood vessels, such as
with spinal cord injury (esp. cervicalspine injury), spinal anesthesia or severe
vasovagal reactions caused by pain or
psychic trauma
DISTRIBUTIVE SHOCK
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DISTRIBUTIVE SHOCK*Septic Shock
- endotoxinmediated,
exotoxin
mediated
Widespread sepsis from gram-
negative or gram-positiveorganisms. Toxins produce
vasodilation & peripheral pooling.
Mediators of inflammationpotentiate the vasodilation. SNS
response cannot overcome
vasodilation. Capillary endothelial
damage, microemboli, myocardial
depression & organ failure are
common effects.
DISTRIBUTIVE SHOCK
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DISTRIBUTIVE SHOCK*Anaphylactic Shock
- IgE mediated:certain drugs, foods,
insect venoms,
pollens
-Non-IgE mediated:iodinated contrast
material, dextran,
opiates, mannitol,
NSAIDs, polymixin B,BT to IgA-deficient
patients, & local
anesthetic
Drastic, acutely developing &
progressing type of shock.Occurs with IgE mediated reactions.
Molecules of IgE bind with allergen &
tissue mast cells, releasing histamine ,
which causes vascular permeability &smooth muscle constriction . Occurs
on re-exposure to an antigen. Non-IgE
mediated reactions can be induced on
first contact. Physiologic response isvasodilatation, & peripheral edema &
bronchoconstriction, SNS cannot
overcome vasodilating stimulus.
Neurogenic Shock(Vasogenic)
Septic Shock-immuno
Anaphylactic Shock-Penicillin sensitivity
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Precipitating event
VasodilationActivation of
inflammatory
response
Decreased venous
return
Maldistribution of blood volume
(Vasogenic)
-Spinal cord injury
-spinal anesthesia
-depressant action of medications
-glucose deficiiency
immuno
suppression
-extremes of age (<1
yr. & >65 yr.)-malnourishment
-chronic illness
-invasive procedures
Penicillin sensitivity
-Transfusion reaction
-Bee sting allergy
-Latex sensitivity-Severe allergy to some
foods or medications
Decreased cardiac
output
Decreased tissue
perfusion
Management of DISTRIBUTIVE SHOCK
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gEtiology Clinical Situation Intervention
Anaphylactic
shock
Allergy to food,
medicines, dyes,insect bites, stings,
or latex
Prepare for surgical management
of the airwayDecrease further absorption of
antigen (stop IV fluid, place
tourniquet between injection or
sting site)Epinephrine (1:100) 2 inhalations
q3O or
Epinephrine (1:1000) 0.2-0.5ml q
5mins. Given at a rate of 1mg/min
IV fluid resuscitation with
isotonic solution
Diphenhydramine HCL or H1 –
receptor antagonist IV
Management of DISTRIBUTIVE SHOCK
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gEtiology Clinical Situation Intervention
Anaphylactic
shock
Allergy to food,
medicines, dyes,insect bites, stings,
or latex
Theophylline IV drip for
bronchospasmSteroids IV
Vasopressors (norepinephrine,
metaraminol bitartrate, high
dosage dopamine)Gastric lavage for ingested
antigen
Ice pack to injection or sting site
Meat tenderizer paste to sting
site
Management of DISTRIBUTIVE SHOCK
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gEtiology Clinical Situation Intervention
Septic shock Often gram-
negative septicemiabut also caused by
other organisms in
debilitated,
immunodeficient orchronically ill
patients
Identify origin of sepsis; culture
all suspected sourcesVigorous IV fluid resuscitation
with normal saline
Empirical antibiotic therapy until
sensitives are reportedIf suspected organism is gram-
positive, vancomycin is used; if
gram-negative, give expanded
spectrum penicillin or a
cephalosporin & aminoglycoside
Administer cardiotonic agents
(dopamine or dobutamine,
norepinephrine, isoproterenol,
digitalic, calcium)
Management of DISTRIBUTIVE SHOCK
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gEtiology Clinical Situation Intervention
Septic
shock
Often gram-
negativesepticemia but
also caused by
other organisms
in debilitated,immunodeficient
or chronically ill
patients
Naloxone (narcotic antagonist) --
capillary bed vasodilationProstaglandins
Monoclonal antibodies
Temperature control (both
hypothermia & hyperthermia arenoted)
Heparin, clotting factors, blood
products if DIC develop
Neurogenic
shock
Spinal anesthesia
Spinal cord injury
Normal saline to restore volume
Treat bradycardia with atropine
Vasopressors (norepinephrine,
metaraminol bitartrate, high dosage
dopamine, phenylephrine
Place in modified trendelenburg position
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SHOCK
Inadequate
tissue/organ
perfusion
affecting all
organs of body
Failure of compensatory mechanisms
Damage to
the capillaryendothelial
lining
Activation of
clotting factors
Lead to complications
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Drug Therapy in Shock
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Vasoconstrictors Vasodilators
To maintain normal BP:
NorepinephrineEpinephrine
Dopamine
Dobutamine
To improve circulation:
NitroglycerineHydralazine
Na bicarbonateTo reverse acidosis:
Antibiotics – sepsis
Heparin – DIC
Steroids – to reduceantiinflammatory effect
Glucagon – to increase
blood sugar
Cimetidine – to prevent stress ulcer
Naloxene (Narcan) – to block endorphin –
mediated hypotension
Diphenhydramine (Benadryl) – foranaphylaxis
Narcotics – to relieve pain (used with
great care because these may cause
respiratory depression)
Drug Therapy in Shock
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g pyCardiotonic Medications
To improve myocardial contraction:Digitalis – evidence of cardiac failure
Amiodarone, lidocaine, bretylium, quinidine, &
procainamide – to treat dysrhythmias that tend toreduce cardiac efficiency
Atropine – may treat bradycardia
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QUESTIONS
1. Which of the following best describes
neurogenic shock?
a. Results from circulating volume
b. Results from compromised cardiac output
c. Results from loss of vasomotor tone that
includes arteriolar & venous dilatation
d. Results from severe allergic reaction
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• Answer: letter c
- neurogenic shock results from loss of
vasomotor tone that includes arteriolar &
venous dilation
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2. During the initial stage of shock, the
following manifestations are expected
EXCEPT:
a. Elevated BP, elevated temperature
b. Tachycardia, restlessness
c. Tachypnea, respiratory alkalosis
d. Diaphoresis, pallor
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• Answer: Letter a
- Elevated BP, elevated temperature are not
expected manifestations during initial stage of
shock. There is hypotension & decreased bodytemperature
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3. During the decompensated stage of shock,the following signs and symptoms occur
EXCEPT:
a. oliguria
b. elevated BUN
c. hyperkalemia
d. metabolic alkalosis
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• Answer: letter d
- metabolic alkalosis is not expected during
decompensated stage of shock. Instead
metabolic acidosis occurs. This is due to bloodstasis that enhances lactic acid production
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4. The following are causes of altered LOC inshock EXCEPT:
a. cerebral hypoxia
b. acidosis
c. accumulation of waste products
d. release of blood from the liver
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• Answer: letter d
- release of blood from the liver is not a cause
of altered LOC in shock. Cerebral hypoxia,
acidosis, accumulation of waste products arecauses of altered LOC in shock
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5. The desired position during shock is:
a. Modified trendelenburg
b. Flat position
c. Semi – Fowlers’s position
d. Lateral position
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• Answer : letter a
- Modified trendelenburg is the desired position
of the client during shock. The patient is placed in
supine position with the legs elevated at 20-30degree angle, the hips slightly higher than the
torso. To increase venous return to the heart & to
strengthen contractility of the heart. Provide
head pillow support to prevent cerebral venous
congestion & an increase ICP
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6. The most commonly used plasma expander is:
a. 0.9% NaCl
b. Dextran
c. Lactated Ringer’s
d. Whole blood
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• Answer: letter b
- Dextran is most commonly used plasma
expander
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7. Which of the following is administered toreverse acidosis?
a. Na bicarbonate
b. Heparin
c. Steroids
d. Cimetidine
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• Answer: Letter a
- Sodium bicarbonate is administered to
reverse acidosis
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8. Hypovolemic shock occurs when blood loss is:
a. 5% - 10%
b. 15% - 25%
c. 10% - 15%
d. 1% - 5%
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• Answer: letter b
- hypovolemic shock occurs when blood loss is
15% - 25%
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9. The client has intra-aortic ballooncounterpulsation device. This is primarily
meant to:
a. decrease cardiac workload
b. decrease stroke volume
c. increase preload
d. maintain current coronary circulation
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• Answer: letter a- intra-aortic balloon counterpulsation deviceincreases coronary artery and myocardial
tissue perfusion & reduces left ventricularworkload. During diastole, the balloon isinflated to allow more blood from the aorta tofill the coronary artery. During systole, the
balloon is deflated to allow free flow of bloodvia the aorta
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10. The following are assessment parametersthat indicate adequate fluid replacement in
shock EXCEPT:
a. urine output is 50 ml/hr
b. CVP = 10cm water
c. Hct = 48 vol. %
d. Serum potassium = 6 mEq/L
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• Answer: letter d
- serum potassium of 6mEq/L is elevated.
This may indicate dehydration, causing
retention of electrolytes. Therefore, fluidreplacement is not adequate.
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