Interventions for Clients with Shock

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Interventions for Clients with Shock

• Esmeralda Garza RN,MSN
• South Texas College

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Whats happening

• Client is a 25 year old married woman with two
  children who provides day care for preschool
  children. As she is driving in the interstate at
  65 miles per hour, a car crosses the median and
  strikes her vehicle head on. Client is not
  wearing seat belt is thrown forward against
  steering wheel. The front of the car is pushed up
  against her by the car that struck her,
  entrapping her lower ext.
• b/p80, pulse120, rr36, on arrival she states she
  is having difficulty breathing.

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Objectives

• Describe the pathophysiology of shock
• Anaylsis the different types of shocks
• Describe the compensatory mechanisms of shock
• Assess clients at risk for shock
• Describe treatments and nursing process
  utilization in care of client with shock
• Develop a care plan for client with shock

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What is shock?

• Shock is the whole-body response to poor tissue
  oxygenation, is a condition rather than a
  disease.
• Any problem that impairs oxygen delivery to the
  tissues and organs can start shock syndrome and
  lead to a life threatening emergency.
• Is a clinical syndrome characterized by a
  systemic imbalance between oxygen supply and
  oxygen demand.

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What happens?

• Shock is the net result of a problem With
• The pump
• The vessels
• The volume

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Prevalence/Incidence

• Incidence exactly is unknown
• Cardiogenic shock presents in 6 to 9 of acute
  MIs and 300,000 occurred between 1995-2004
• 80 of cardiogenic shock cases are fatal
• Distributive shock from sepsis has a mortality
  rate40 to 85.

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• Review
• of
• tissue
• perfusion

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Normal Regulation of BP

• Stroke volume the amount of blood ejected by the
  left ventricle during each systole.
• Cardiac Output
• Cardiac Output heart rate X stroke volume
• CO-Normal range _____ liters/min.
• BP the force of the arterial blood exerted
  against the vessel walls

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Factors Influencing MAP
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Key features of SHOCK

• CARDIOVASCULAR
• Decreased cardiac output
• Increased pulse rate
• Thready pulse
• Decreased blood pressure
• Narrowed pulse pressure
• Postural hypotension
• Low central venous tension
• Flat neck veins
• Slow capillary refill
• Diminished peripheral pulses

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Key features of shock

• RESPIRATORY
• Increased respiratory rate
• Decreased PaCO2
• Decreased PaO2
• Cyanosis around lips and nail beds

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Key features of shock

• Neuromuscular
• EARLY
• Anxiety
• Restlessness
• Increased thirst
• Late
• Decreased CNS activity coma
• Generalized muscle weakness
• Sluggish pupillary response to light

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Key features of SHOCK

• RENAL MANIFESTATIONS
• Decreased urinary output
• Increased specific gravity
• Sugar and acetone present in urine

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Key features of SHOCK

• INTEGUMENTARY
• Cool to cold
• Pale to mottled to cyanotic
• Moist, clammy
• Mouth dry, pastelike coating
• GASTROINTESTINAL
• Decreased motility
• Diminished or absent bowel sounds
• Nausea and vomiting
• constipation

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Stages of SHOCK-INITIAL

• This is where the hypoperfusional states causes
  hypoxia, leading to the mitochondria being unable
  to produce adenosine triphosphate. Due to this
  lack of oxygen, the cell membranes become damaged
  and the cells perform anaerobic respiration. This
  causes a build-up of lactic and pyruvic acid
  which results in systemic metabolic acidosis.
  These harmful compounds require to be removed
  from the cells, primarily by the liver, however
  this process requires oxygen.

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Compensatory

• - This stage is characterised by the body
  employing physiological mechanisms, including
  neural, hormonal and bio-chemical mechanisms in
  an attempt to reverse the condition. As a result
  of the acidosis, the person will begin to
  hyperventilate in an attempt to inspire more
  oxygen. The baroreceptors in the arteries detect
  the resulting hypotension, and cause the release
  of adrenaline and noradrenaline. These cause
  widespread vasoconstriction resulting in an
  increase in not only blood pressure but heart
  rate. Also, these hormones cause the
  vasoconstriction of the kidneys, gastrointestinal
  tract, and other organs to divert blood to the
  heart, lungs and brain. The lack of blood to the
  renal system causes the characteristic low urine
  production.

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PATHOPHYSIOLOGY OF SHOCK SYNDROME

• Cells switch from aerobic to anaerobic metabolism
  
• lactic acid production
• Cell function ceases swells
• membrane becomes more permeable
• electrolytes fluids seep in out of cell
• Na/K pump impaired
• mitochondria damage

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COMPENSATORY MECHANISMS Sympathetic Nervous
System (SNS)-Adrenal Response

• SNS - Neurohormonal response Stimulated by
  baroreceptors
• Increased heart rate
• Increased contractility
• Vasoconstriction (SVR-Afterload)
• Increased Preload

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COMPENSATORY MECHANISMS Sympathetic Nervous
System (SNS)-Adrenal Response

• SNS - Hormonal Renin-angiotension system
• Decrease renal perfusion
• Releases renin angiotension I
• angiotension II potent vasoconstriction
• releases aldosterone adrenal cortex
• sodium water retention

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COMPENSATORY MECHANISMS Sympathetic Nervous
System (SNS)-Adrenal Response

• SNS - Hormonal Antidiuretic Hormone
• Osmoreceptors in hypothalamus stimulated
• ADH released by Posterior pituitary gland
• Vasopressor effect to increase BP
• Acts on renal tubules to retain water

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Failure of Compensatory Response

• Decreased blood flow to the tissues causes
  cellular hypoxia
• Anaerobic metabolism begins
• Cell swelling, mitochondrial disruption, and
  eventual cell death
• If Low Perfusion States persists
• IRREVERSIBLE DEATH IMMINENT!!

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Progressive

• - Should the cause of the crisis not be
  successfully treated, the shock will proceed to
  the progressive stage and the compensatory
  mechanisms begin to fail. Due to the decreased
  perfusion of the cells, sodium ions build-up
  within while potassium ions leak out. As
  anaerobic metabolism continues, increasing the
  body's metabolic acidosis, the arteriolar and
  precapillary sphincters constrict such that blood
  remains in the capillaries. Due to this, the
  hydrostatic pressure will increase and, combined
  with histamine release, this will lead to leakage
  of fluid and protein into the surrounding
  tissues. As this fluid is lost, the blood
  concentration and viscosity increase, causing
  sludging of the micro-circulation. The prolonged
  vasoconstriction will also cause the vital organs
  to be compromised due to reduced perfusion.

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REFRACTORY

• At this stage, the vital organs have failed and
  the shock can no longer be reversed. Brain damage
  and cell death have occurred. Death will occur
  imminently.

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Multiple organ dysfunction syndrome

• Massive release of toxic enzymes
• MODS
• Dead cells trigger clots(microthrombi) form.
• Clots block tissue oxygenation damage more cells
• Cycle continues
• Treatment
• Xigris

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Whos at Risk

• The very young or the very old.
• Post MI clients
• Clients with severe dysrhythmia
• Persons with a recent hemorrhage or blood loss
  history.
• Clients with burns.
• Clients with massive/overwhelming infections.

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• Causes or types
• of
• shock

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HYPOVOLEMIC SHOCK

• A decrease of intravascular volume of 15 or more
• Stroke volume, cardiac output and b/p decrease
• Most common type of shock

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May result from

• Loss of blood volume from hemorrhage
• Loss of intravascular fluid from the skin due to
  injuries such as burns
• Loss of blood volume from severe dehydration
• Loss of fluid from the GI system
• Renal losses of fluid due to diuretics or DI
• Conditions causing fluid shifts from
  intravascular compartment to interstitial space
• Third spacing,liver disease, pleural effusion

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Overall causes

• Trauma
• GI ulcer
• Surgery
• Dehydration
• Vomiting
• Diarrhea
• Diuretic therapy
• NGT suction
• Diabetes Insipidus
• Hyperglycemia

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• Nursing
• Process

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Case Study

• You are working in an outpatient clinic when a
  mother brings in a 25 year old daughter ch who
  has type 1 diabetes mellitus and has returned
  from a trip from Mexico.
• She had a 3day fever of unknown origin diarrhea
  N/V.
• Unable to eat or drink
• Has taken her insulin
• Unsteady, skin warm,flushed, respiration deep,
  rapid, pulse rapid thready, feels dizzy, and
  thirsty.

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Appropriate or Inappropriate

• -1000 ml LR stat
• -Give 36 units lente and 20 regular sq
• -lab work
• -1800cal ADA diet
• -Ambulate quid
• -tylenol 650mg po
• -lasix 60mg IV now
• -urine output q hour
• -vs q shift.

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History-age Ht wt, other changes
C O L L A B O R A T I V E M A N A G E M E N T
ASSESSMENT

• Physical Assessment
• Cardiovascular, Skin,
• Neurologic, Renal

25-year old client cc severe vomiting
Psychosocial Assessment
Laboratory Assessment
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Treatment

• Airway
• Breathing
• Circulation
• Vascular Access
• IO/IV
• Isotonic fluid
• Inotropes, vasoactive medications

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Treatment

• Goal is early intervention to prevent
  irreversible organ damage
• Recognize early shock
• Diagnose and correct the underlying cause

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P L A N N I N G I M P L E M E N T A T I O N

• Fluid Management
• Diet therapy
• Drug therapy

• Deficient fluid volume
• r/t excessive fluid loss
• Maintain BP WNL
• IO
• Urine specific gravity
• lt1.030
• - Good skin turgor

• Fluid monitoring
• Drug therapy
• Oxygen therapy

• Decreased cardiac output
• r/t decreased plasma
• volume
• BP and PR are WNL
• UO of at least
• 30 ml/hr

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Cardiogenic Shock

• Client is a 50 year old executive. He is five
  feet 10 inches tall and weighs 225 lbs. Smokes,
  on statins, acid reducer for indigestion, drinks
  occassionally does not exercise.
• Bouts of chest pressure, chest pain
  sweating,shortness of breath.
• b/p160/86 hr122rr30 pulse ox88
• Has an MI
• b/p 80/66 hr 142, rr36 pulse ox 91
• Arteral abg 7.67-28-80-40

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Cardiogenic Shock

• Occurs when actually heart muscle is unhealthy
  and pumping is directly impaired
• Causes include
• MICardiac arrest
• Ventricular dysrhythmias
• Cardiomyopathies

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Manifestations

• Blood pressure hypotension
• Pulse rapid thready
• Respirations increased labored crackles wheezes
  pulmonary edema
• Skin pale cyanotic
• Mental status restless anxious lethargic
• Urine output oliguric to anuric
• Other dependent edema, elevated cvp elevated pcwp
  arrhythmia.

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C O L L A B O R A T I V E M A N A G E M E N T
History
Physical Assessment
Cardiogenic Shock
Psychosocial Assessment
Laboratory Assessment
Radiographic Assessment
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What is the Nursing process?

• Interventions
• ASA 325mg
• Lopressor 5mg IV every 5 minutes for three doses
• Dopamine 10mcg/kg/min
• Dobutrex 10mcg/kg/min
• Oxygen

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Collaborative management

• Maximize oxygen delivery to the tissue. Monitor
  abg. Hgb and cardiac output. Intubation and
  mechanical ventilation.
• Optimizing cardiac contractility and cardiac
  output. Pulmonary artery catheter ekg
  neurological assessment
• Recognize risk and benefits of inotropes,
  vasopressors, vasodilators and analgesics and
  diuretics
• Maintain bedrest
• Administer deep vein thrombosis prophylaxis
• Avoid overheating
• Correct metabolic acidosis

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• Treating pain and anxiety
• Providing patient and family support
• Atttending to nutritional needs
• Maintaining renal perfusion
• Care of IABP
• Care of pre post angiogram
• Care of prepost CABG

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So question

• The most common etiology for cardiogenic shock is
• A. pulmonary embolus
• B. hypovolemic shock
• C. neurogenic shock
• D. Acute MI

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OBSTRUCTIVE SHOCK

• This is caused by an obstruction in the heart or
  great vessels the either impedes venous return or
  prevents cardiac pumping action.
• Causes include
• Cardiac tamponade
• Arterial stenosis
• Pulmonary embolus
• Pulmonary hypertension
• Thoracic tumors
• Tension pneumothorax

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C O L L A B O R A T I V E M A N A G E M E N T
History
Physical Assessment
Obstructive Shock Cause Pneumo Etc.
Psychosocial Assessment
Laboratory Assessment
Radiographic Assessment
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• DISTRIBUTIVE
• SHOCK

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• A 39 year old man presents cool and clammy skin,
  a b/p of 88/60 mmHG,and a fever of 104.5. He has
  been fighting a bacterial infection for 3 days.
  He has had a foley catheter for 1 month. Urine is
  cloudy and foul smelling.

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What happens?

• There is los of sympathetic tone, blood vessel
  dilation, pooling in venous and capillary beds
  and increased blood vessel permeability.
• Also called

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DISTRIBUTIVE SHOCK

• ANAPHYLACTIC SHOCK
• NEUROGENIC SHOCK
• SEPTIC SHOCK

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Neural induced distributive shock

• Loss of MAP occurs when sympathetic nerve
  impulses controlling blood vessel smooth muscle
  are decreased resulting in vaso dilation.

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Chemical induced

• Has three origins-anaphylaxis, sepsis, and
  capillary leak syndrome.
• Chemicals change blood vessel walls.

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C O L L A B O R A T I V E M A N A G E M E N T
History
Physical Assessment
Distributive shock
Psychosocial Assessment
Laboratory Assessment
Radiographic Assessment