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SHOCK

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BP rises and skin is cold and clammy due to peripheral vasoconstriction ... cool, clammy skin. pale or cyanotic color. Cardiogenic Shock. Coarse rales in the lungs ... – PowerPoint PPT presentation

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Title: SHOCK


1
SHOCK
  • Presented
  • by
  • Harmon P. Mercer
  • RN,MS,CCRN

2
Shock
  • Purpose To provide the critical care
  • nurse with the knowledge and skills necessary
    to manage the care of patients experiencing shock
    in the critical care setting.

3
Shock Objectives
  • 1. Define shock
  • 2. Differentiate among hypovolemic, cardiogenic,
    anaphylactic, neurogenic, and septic shock.
  • 3. Describe the pathophysiology of shock.
  • 4.Compare the four stages of shock and
    associated signs and symptoms.

4
Shock Objectives
  • 5. Relate the s/s of shock to neural, hormonal,
    chemical compensatory mechanisms.
  • 6.Discuss the pharmacokinetics of dopamine,
    dobutamine, epinephrine, nor-epinephrine,
    sodium nitroprusside in the resuscitation of the
    patient in shock.
  • 7. Explain the goals of treatment for patients
    in shock.

5
SHOCK
  • Definition
  • Acute wide spread impaired tissue perfusion
  • Circulatory collapse which leads to hypoperfusion
    hypoxia
  • Cellular, metabolic and hemodynamic
    disarrangements occur

6
Shock
  • Shock is defined as inadequate perfusion to the
    tissues of the body
  • The body isnt getting enough oxygen or nutrients
    to feed itself. 
  • There are different types of shock and though
    they are all similar, they act upon the body in
    different ways.

7
Clinical Manifestations of Shock
  • Differ according with the stage
  • Try to improve tissue perfusion
  • Depends on how much O2 is available
  • If it is transported to the tissues
  • If they are able to use it.

8
Clinical Manifestations of Shock
  • This is affected by Hb level, cardiac output and
    pulmonary gas exchange
  • Hb and cardiac output are going to depend on the
    HR, preload, afterload and contractility

9
How does it happen?
  • Shock is a process that happens on a cellular
    level. 
  • Most forms of shock are caused by inadequate
    delivery, which means the body doesnt have the
    adequate amounts of oxygen or nutrients it needs
    to survive

10
How does it happen?
  • Some are caused by inadequate utilization,
    meaning the body has what it needs to survive, it
    just doesnt know how to use it. 
  • Shock, if not quickly recognized and rapidly
    reversed, will be fatal.

11
Shock
  • Causes
  • Decrease volume or loss of intravascular volume
    (Hypovolemic)
  • Decrease cardiac output or Impaired myocardial
    function (Cardiogenic)
  • Maldistribution of intravascular volume
    (Distributive)

12
Maldistribution of intravascular volume
(Distributive)
  • Severe antibody antigen reaction (Anaphylactic)
  • Loss of sympathetic tone (Neurogenic)
  • Microorganisms invading body systems (Septic)

13
The Four (4) Stages of Shock
  • Initial Stage ? cardiac output, impaired tissue
    perfusion.
  • As blood supply to tissues ? ? aerobic
    metabolism for a short period ? anaerobic
    metabolism to get some energy? byproducts are
    produced? acid lactic formation ? cellular damage

14
Initial Stage
  • CO ?
  • ? ? ?
  • Impaired tissue Perfusion
  • ? ? ? ?
  • Anaerobic Metabolism
  • ? ? ? ?
  • Lactic acidemia
  • ? ? ? ?
  • Cellular damage

15
STAGES OF SHOCK Stage of Compensation
  • Stage of Compensation (sympathetic activates ?
    cool, pupils dilated etc)
  • Pathway
  • Decreased cardiac output leads to reflex
    sympathetic stimulation causing increase HR and
    peripheral vasoconstriction

16
STAGES OF SHOCK Stage of Compensation
  • Pathway
  • BP rises and skin is cold and clammy due to
    peripheral vasoconstriction
  • Urine output drops (oliguria) due to renal artery
    vasoconstriction

17
Stage Of Compensationcont.
  • Compensatory Stage the body is trying to improve
    the tissue perfusion. The sympathetic NS ?
    Neural, hormonal chemical responses.
  • Neural
  • ? HR, ? heart contractility, arterial and venous
    vasoconstriction ? blood is going to be shunted
    to the body organs

18
Stage Of Compensationcont.
  • Hormonal
  • Renin response ? angiotensin II ? Aldosterone ?
    ADH this is going to retain H2O and Na
  • Anterior pituitary ? ACTH ? adrenocortex is
    stimulated ?glucocorticoids ? ? glucose
  • Adrenal medulla stimulation ? epinephrine
    norepinephine

19
Stage Of Compensationcont.
  • Chemically
  • Epinephrine causes an increase in HR/Cardiac
    contractility and therefore tissue perfusion
  • Norephrine causes arterial vasocontriction and
    shunts blood away from non vital organs to vital
    organs.
  • The response of the Pt is to hyperventilate ? it
    tries to do is to neutralize the lactic acidosis

20
Stage Of Compensationcont.
  • Neurologic
  • ? ? ?
  • Sympathetic
    Chemoreceptors
  • ? ? ? ?
    ? ?
  • Vasoconstriction ? HR ?Rate/Depth
  • Contractility
    Respiration
  • ? ?
    ?
  • Shunting of ? CO
  • Blood
    ?PaCo2

    Tissue
  • Perfusion
    Respiratory Alkalosis

21
Stage Of Compensationcont.
 
 
  • Endocrine
  • ? ? ? ?
  • RAS ACTH
  • ? ? ? ? ? ?
  • Vasoconstriction
    Glucorticoid

    Na and H2 ? ?
  • retention
    ? Serum

  • Glucose

22
Stage of Progression
  • Progressive Stage the compensatory mechanisms
    are starting to fail
  • Na K pump and the cellular membranes fail ?
    cellular death (rupture) and then every system in
    the body is affected
  • Cardiac Pt ? ventricular failure
  • Neurologically ? cerebral hypoperfusion
  • Thermoregulation failure

23
Stage of Progression cont.
  • Coma
  • Pulmonary ? Acute respiratory failure
  • Renal ATN, renal vasoconstriction, renal
    hypoperfusion
  • Disseminated Intravascular Coagulation (DIC)
  • GI gram-negative bacteria enter into the system
  • Hepatic pancreatic failure

24
Stage of Impaired Perfusion (Progressive Shock)
  • Pathway
  • Prolonged vasoconstriction causes irreversible
    ischemic injury. Adverse effects that occur as a
    direct consequence of decreased perfusion
  • Anaerobic metabolism of glucose ? lactic acidosis
  • Cell necrosis as in ATN ? acute renal failure

25
Stage of Impaired Perfusion (Progressive Shock)
  • Acute alveolar damage ? intra-alveolar edema,
    hemorrhage and formation of a hyaline-fibrin
    membrane (Shock Lung) ARDS
  • Anoxic necrosis of liver ? Nutmeg Liver
  • Ischemic necrosis of intestines ? release of
    bacterial toxins ? worsening shock

26
Stage of Decompensation
  • Pathway
  • Hypoxia and acidosis ? failure of reflex
    (sympathetic) peripheral vasoconstriction
    (vasodilation) ? progressive hypotension until
    perfusion of heart and brain reach critical
    levels
  • Prognosis for Shock depends upon cause and stage
    at which treatment is begun

27
Stage of Decompensation
  • Initial Stage
  • ? ? ?
  • Compensatory Stage
  • ? ? ? ?
  • Compensatory mechanism begin to fail
  • ? ? ? ?
  • Some irreversible cellular damage

28
Stage of Decompensation
  • The shock cycle begins to perpetuate itself
  • BP and blood flow can not be maintained
  • Anaerobic metabolism cannot sustain cellular
    activity
  • Irreversible cellular damage occurs
  • Organ dysfunction appears

29
Stage of Decompensation
30
Refractory Stage
  • Refractory Stage Irreversible
  • MODS multiple organ dysfunction syndrome
  • Renal ? hepatic ? pulmonary ? cardiac

31
Critical Care Nursing
  • You live by the motto "to be right is only half
    the battle, to convince the doctor is more
    difficult."

32
Types of shock
  • Hypovolemic Circulating or intravascular volume
    loss
  • Hemmorhagic
  • Cardiogenic inability of the heart to pump
  • Distributive maldistribution of circulating
    blood volume
  • Septic
  • Anaphylactic
  • Neurogenic loss of sympathetic tone

33
TYPES OF SHOCK
  • Hypovolemic decreased volume in circulation due
    to
  • Severe hemorrhage
  • GI losses
  • Losses secondary to wound of surgery
  • Burns

34
Hypovolemic Shock
  • This is fluid loss in the intravascular space.
  • It is the most common due to GI bleeding,
    trauma.
  • Two types
  • Absolute and Relative 

35
Hypovolemic Shock
  • Absolute due to trauma, surgery of GI system
    (esophageal varices).
  • Blood, plasma ? loss
  • External loss of fluid 

36
Hypovolemic Shock
  • Relative rupture of spleen, arterial dissection,
    sepsis, hyponatremia, internal injuries that
    cause a shift from the intravascular ?
    extravascular compartments
  • Loss on intravascular integrity
  • ? capillary permeability

37
Hypovolemic Shock
  • Pathology ? of venous return ? ? preload (stroke
    volume cardiac output) Inadequate tissue
    perfusion
  • Initially pt losses about a 15, which is about
    750 ml
  • At 40 or greater BIG TROUBLE

38
Hypovolemic Shock
  • During the compensatory stage we want to maintain
    cardiac output
  • ? Cardiac output tachycardia, pulse narrows, ?
    diastolic pressure, tachypnea
  • ABGs reveal a respiratory alkalosis hypoxemia

39
Hypovolemic Shock
  • ? Urinary output
  • Skin is pale, cool, delayed capillary refill
  • Jugulars are collapse (flat)
  • Neurological change in LOC

40
Hypovolemic Shock
  • In the progressive stage we are going to see a
    1500 2000 ml loss
  • ? HR, myocardial ischemia ?some arrhythmias
  • ABGs ? metabolic acidosis ? PCO2 ?, Bicarbonate ?
    and PaO2 ?

41
Hypovolemic Shock
  • Pt ? acute renal failure where BUN and creatinine
    ?
  • When the organs start failing we are going to see
    the pt becomes hypotensive probably we have to
    administer dopamine, vasopressin

42
Hypovolemic Shock
  • In the Refactory we are going to see ? 2000 ml
    loss
  • Severe tachycardia and then bradycardia
  • ? Preload (right atrial pressure) RAP CVP ?
  • ? Stroke volume ? tissue perfusion
  • ? Afterload ? ? SVR (systemic vascular
    resistance) 

43
Hypovolemic Shock
  • Management
  • Prevent and correct the fluid loss
  • Restore tissue perfusion
  • 2 peripheral accesses Large bore IVs
  • Triple lumen catheter

    (femoral or jugular))
  •  Administer appropriate fluids
  • Watch for S/S of overload, monitor right atrial
    and PA pressures

44
Hypovolemic Shock
  • Hypovolemic Shock is similar to hemorrhagic
    shock. 
  • The difference is the patient is losing body
    fluid rather than blood. 
  • This body fluid is water and/or plasma. 

45
Hypovolemic Shock
  • This thickens the blood making it difficult for
    the heart to put out enough volume to meet the
    demands of the body. 
  • The most common causes of hypovolemic shock are
    severe dehydration and severe burns. 

46
Hypovolemic Shock
  • Signs and symptoms are the same as hemorrhagic
    shock, but include
  • Collapsed veins in the extremities and neck,
  • Poor skin turgor
  • Concentrated, dark, strong smelling urine.

47
Hemmorhagic Shock
  • Hemmorhagic Shock is when the body is losing
    blood volume. 
  • When it loses this volume, the red blood cells
    which carry the oxygen are depleted

48
Hemmorhagic Shock
  • The blood loss may be caused from a traumatic
    source, and may be quite obvious because there is
    a copious amount of blood around the body
  • i.e. GSWs , stab wounds, large
    lacerations,
  • amputations,etc. 

49
Hemmorhagic Shock
  • The traumatic source may also be from blunt
    trauma where the injury is an organ that has torn
    or ruptured. 
  • This can be the result of being hit with a blunt
    object like a baseball bat, slamming into the
    steering wheel in a vehicle crash or falling any
    distance. 

50
Hemmorhagic Shock
  • The solid organs of the body are the organs that
    usually tear or rupture from an impact. 
  • The solid organs in the abdomen are the liver and
    kidneys, spleen (LUQ, under the rib cage), and
    appendix (RLQ). 

51
Hemmorhagic Shock
  • With a blunt trauma injury, the patient is losing
    blood inside their body. 
  • A person can bleed into three areas of their
    body the chest cavity, the abdominal cavity, and
    into both thighs
  • e.g. bilateral femur
  • fractures. 

52
Hemmorhagic Shock
  • Hemmorhagic shock can also be caused from an
    atraumatic bleed commonly caused from bleeding
    ulcers. 

53
Hemmorhagic Shock
  • Signs and symptoms with hemorrhagic shock are
    what most people think of as shock
  • low blood pressure (systolic below 100),
  • high pulse rate (above 120), and
  • rapid respiratory rate (greater than 32),
  • the skin will be pale or cyanotic, cold and
    sweaty. 

54
Cardiogenic Shock
55
TYPES OF SHOCK
  • Cardiogenic A form of shock resulting from the
    hearts failure to inadequately pump blood.
  • This results in inadequate delivery of oxygenated
    blood to the periphery, there tissue perfusion is
    also inadequate.

56
Cardiogenic Shock
  • Cardiogenic Shock may result from many different
    etiologies
  • Ventricular Ischemia caused by
  • Acute MI
  • Open Heart Surgery
  • These are the most
    common 

57
Cardiogenic Shock
  • Structural Defects
  • Papillary muscle rupture
  • Cardiomyopathy
  • Pulmonary Embolus
  • Dysrhymthmias
  • Affect normal circulation

58
Cardiogenic Shock
  • Signs and symptoms include
  • chest pains
  • shortness of breath with increased rate
  • cool, clammy skin
  • pale or cyanotic color

59
Cardiogenic Shock
  • Coarse rales in the lungs
  • Cardiac dysrhythmias
  • Hypotension
  • tachycardia

60
Cardiogenic Shock
  • ? CO/CI
  • ? PA and PAWP
  • ? SVR
  • Cardiac Enzymes
  • ?UO

61
Pathophysiology
  • Failure to eject blood
  • from ventricles
  • ?
  • Increased Pulmonary
  • Pressures
  • ?
  • Pulmonary Congestion
  • ?
  • Hypoxemia

Ineffective Pumping of Blood
? SV ? CO
Inadequate tissue perfusion
62
Cardiogenic Shock
  • Treat Underlying cause
  • Thrombolytics,angioplasty, surgery,antiarrhythmics
    ,electrical therapy
  • ? Pumping effectiveness
  • Vasodilators, diurectics, inotropes, mechanical
    devices

63
Cardiogenic Shock
  • Improve tissue perfusion O2, activity
    restriction,analgesics, sedatives
  • Monitor hemodynamics, enzymes, electrolytes, IO,
    ABGs, ECG

64
(Distributive shock) Anaphylactic Shock
  • Severe hypersensitive reaction which leads to
    (antigen antibody) response. ?
  • ? Tissue perfusion and shock syndrome occurs as a
    consequence 

65
Distributive Shock Anaphylactic Shock
  • Risk factors
  • Food allergies
  • Insulin
  • Vaccines
  • Drugs
  • Venoms (snakes, spiders etc)
  • Blood transfusions
  • Environmental agents
  • Latex

66
Distributive Shock Anaphylactic Shock
  • It is an Ig E or non Ig E mediated response 
  • ? Capillary permeability
  • Bronchoconstriction
  • Excessive mucous production
  • Coronary vasoconstriction
  • Inflammation
  • Cutaneous skin reactions
  • Constriction of intestinal wall, bladder uterus

67
Pathophysiology
Exposure Antigen Antibody response
Increased Capillary Permeability
Vasodilation
? Circulating volume ? Decrease CO
? Inadequate Tissue perfusion
68
Anaphylactic Shock
  • Treatment
  • Maintain adequate airway
  • Consider mechanical ventilation
  • Circulation
  • insert large bore IV give fluids
  • Medications-
  • epinephrine, antihistamines, bronchodilators,
    steroids
  • Educate patient

69
Distributive Shock Anaphylactic Shock
  • S/S
  • It starts 15 30 minutes with generalized
    itching, redness and angioedema.
  • Give epinephrine ? most prominent actions are on
    the heart, producing a rapid rise in blood
    pressure, increased strength of ventricular
    contraction, increase in the heart rate, and
    constriction of the arterioles in the skin and
    mucosa.

70
Distributive Shock Anaphylactic Shock
  • Epinephrine relaxes the smooth muscles of the
     bronchi.
  • It elevates the blood sugar level by increasing
    hydrolysis of glycogen to glucose in the liver,
    and at the same time begins the breakdown of
    lipids in fat cells.
  • Epinephrine has a suppressive effect on the
    adaptive immune system.

71
Distributive Shock Anaphylactic Shock
  • Epinephrine
  • It is the drug of choice in anaphylaxis.
  • Dose 0.1 mg/Kg of a 110000 dose, usually given
    IV in 3 5 minutes push.
  • If pt is intubated we can put it down the tube.

72
Neurogenic Shock
  • Neurogenic rare occurrence resulting from loss
    sympathetic tone and is caused by an injury of
    the spinal cord above T6.
  • Loss or suppression of sympathetic tone, the
    onset is between minutes but can last for days,
    weeks or months, depending on the cause

73
Neurogenic Shock (Distributive shock)
  • S/S
  • ? BP
  • Bradycardia
  • Skin warm dry 
  • Determine the cause to treat it
  •  

74
Neurogenic Shock
  • Signs and symptoms
  • low blood pressure,
  • increased respiratory rate,
  • diaphragmatic breathing (quadriplegia (total
    loss of sensation and movement from the neck
    down).  
  • Rarely is neurogenic shock reversible.

75
Neurogenic Shock (Distributive shock)
  • Risk Factors
  • Spinal cord injuries above the level of T6
  • Spinal anesthetic
  • Emotional stress
  • Pts with intractable pain
  • Pts with CN system dysfunction

76
Neurogenic Shock (Distributive shock)
  • Pathology
  • When we loss sympathetic tone we have
  • Massive peripheral dilatation
  • Impaired thermal regulation

77
Neurogenic Shock (Distributive shock)
  • Arterial and venous vasodilatation
  • ? Venous return ? ? preload ? ? CVP
  • ? Arterial return ? ? afterload ? ? BP ?
  • ? SVR systemic vascular resistance

78
Pathophysiology
Loss of sympathetic tone
Loss of thermoregulation
Massive Vasodilation ? CO
Inadequate Tissue Perfusion
Bradycardia
79
Septic Shock
  • Septic Shock Secondary to gram negative sepsis
    due to endotoxemia causing direct toxic vessel
    injury
  • PathwayVasodilatation leads to peripheral
    pooling and relative hypovolemia and decreased
    perfusion

80
Septic Shock
  • Septic Shock is when an infection has invaded the
    body and causes the cells to be unable to utilize
    oxygen and nutrients. 
  • Often intense intravenous antibiotic therapy is
    required and even then may not be effective. 

81
Pathology
  • Gram-negatives release endotoxins from their cell
    membrane as they lyse and die. Gram-positive
    bacteria release exotoxins throughout their life
    span.
  • These toxins trigger the release of cytokines
    (proteins release by cells to signal other cells)
    such as tumor necrosis factor and the
    interleukins.
  • They also activate phagocytic cells as the
    macrophages.

82
Pathology
  • Microorganism invades the CNS endocrinal system
  • Sympathetic nervous system is stimulated and
    release ACTH (epinephrine norepinephine,
    glucocorticoids, aldosterone, glucagons and
    renin) ? after release ? hypermetabolic state ?
    massive peripheral dilatation, form of
    microemboli, selective vasoconstriction ?
    capillary membrane ? ? tissue perfusion, ?
    cellular perfusion ? acid lactic as a result of
    metabolic metabolism

83
Pathology
  • These complex chemical reactions lead to multiple
    system effects ? MODS
  • Microorganism invasion ? inflammatory immune
    response ? endothelium damage? cellular hypoxia

84
Septic Shock (Distributive shock)
  • Most frequent
  • Maldistribution of blood flow (some areas ?
    perfusion and on others ? the perfusion)
  • Increased blood will occur to the heart, brain,
    liver and adrenal glands.
  • At the same time therell be a decrease in blood
    to the skin, lungs, kidneys and viscera.
  •  

85
Septic Shock (Distributive shock)
  • It is a sepsis-induced shock with hypotension
    despite adequate fluid replacement that produce
  • Mortality rate gt 45 depending on the population
    age
  • Primary source is gram-negative positive
    bacteria , aerobes and anaerobes, fungi or viral.
  • Gram-negatives are more frequent

86
Septic Shock (Distributive shock)
  • Risk Factors
  • Diabetes
  • Malnutrition
  • Alcohol abuse
  • Cirrhosis
  • Respiratory infections
  • Hemorrhage
  • Cancer
  • Surgery

87
Septic Shock (Distributive shock)
  • Risk Factors
  • Traumatic injuries with peritoneal contamination
  • Burns
  • Prolonged IV cannulation
  • Abscesses
  • Multiple blood transfusions

88
Septic Shock
  • 2 types Exogenous and Endogenous 
  • Exogenous (hospitals)
  • Endogenous (skin, GI track, respiratory GU,
    catheters, EGT, ETT)

89
Septic Shock
  • Intrinsically age of pt and comorbidities
  • Extrinsically Drug therapy, fluid therapy and
    surgery
  • Similar to toxic shock syndrome (tampons ?
    gram-positives caused by staphylococcus aureus)

90
Septic Shock (Distributive shock)
  • Venous system dilate ? ? preload both in right
    and left ventricles ?
  • ? RVP
  • ? afterload, ? SVR, ? BP

91
Septic Shock
  • Signs and symptoms include in early stages, high
    blood pressure, high pulse rate and high
    respiratory rate, fever, chills, and sweats. 
  • In late stages, the opposite, low blood
    pressure, low pulse rate, low respiratory rate
    and low body temperature.

92
Three Stages have been identified 
  • Early
  • Hyperdynamic
  • Compensated stage

93
Stages
  • Early
  • Tachycardia
  • ? Cardiac index
  • Skin warm and flushed
  • Normal BP

94
Stages
  • Hyperdynamic stage
  • As shock progresses
  • Diastolic BP ?
  • Pulse widens
  • Peripheral pulses are bounding
  • Temperature can be normal, elevated or below
    normal

95
Stages
  • Late Hyperdynamic, uncompensated
  • Widespread organ dysfunction begins to occur
  • BP ? ? hypotension
  • ? Peripheral edema is more evident
  • Labored Tachypnea
  • Crackles ? pulmonary interstitial edema
  • Sputum copious, pink and frothy

96
Stages
  • Late septic shock
  • BP ? 90 mmHg
  • Cold extremities
  • MODS
  • ? Urinary output
  • Abdominal distention
  • Absence of BS
  • Bleeding from invasive lines ? Disseminated
    intravascular coagulation (DIC)

97
Stages
  • Late septic shock
  • MODS
  • Petechiae
  • Cardiac dysrhythmias
  • ABGsyou will see hypoxemia, hypercapnia
  • Metabolic acidosis (Lactic acidosis)
  • COMA

98
Stages
  • Shift to left of WBC (later)
  • ? of glucose and the pt develops an insulin
    resistance 
  • Obtain blood cultures right away, then initiate
    broad-spectrum antibiotics, when results of the
    cultures return adjust the antibiotics.

99
Treatment
  • Triple antibiotics
  • Without the right antibiotic ? endotoxins ?
    aggravates the case 
  • Drugs
  • Vasoconstrictors (dopamine or norepinephrine
    (Levophed))
  • Platelet aggregated antagonist (Aspirin and
    NSAIDs non-steroidal anti-inflammatory drugs)
  • Steroids shown no benefit

100
Platelet aggregated antagonist
  • Aspirin
  • NSAIDs (non-steroidal anti-inflammatory drugs)
    Ibruprofen
  • Dipyridamole (Persantine )
  • Ticlopidine (Ticlid) and Clopidogrel (Plavix)
  • GPIIB/IIIA Inhibitors
  • Glycoprotein (GP) IIB/IIIA
  • abciximab (Reopro), tirofiban (Aggrastat),
    lamifiban and eptifibatide (Integrilin)

101
XigrisDrotrecogin alfa (activated)
  • Xigrisä (drotrecogin alfa) (activated) is a
    recombinant form of human Activated Protein C.
  • Activated Protein C exerts an antithrombotic
    effect by inhibiting Factors Va and VIIIa.

102
Xigris Easy
  • Xigris is the first drug to receive FDA approval
    for increasing survival in high-risk adult
    patients with severe sepsis.
  • Xigris is a recombinant version of human
    Activated Protein C, which modulates
    microvascular function by decreasing inflammation
    and coagulation and increasing fibrinolysis.

103
What does Xigris do?
  • Activated Protein C has indirect profibrinolytic
    activity through its ability to inhibit
    plasminogen activator inhibitor-1 (PAI-1) and
    limiting generation of activated
    thrombin-activatable-fibrinolysis-inhibitor.
  • Activated Protein C may exert an
    anti-inflammatory effect by inhibiting human
    tumor necrosis factor production by monocytes, by
    blocking leukocyte adhesion to selectins, and by
    limiting the thrombin-induced inflammatory
    responses within the microvascular endothelium.

104
Drugs used in the treatment of Shock
  • Vasoconstrictors epinephrine drips, Levophed,
    neo-synephrine, dopamine
  • A vasoconstrictor is any substance that acts to
    constrict blood vessels, i.e. make the lumen
    narrow, or vasoconstriction. Many
    vasoconstrictors act on specific receptors, such
    as vasopressin receptors or adrenoreceptors.
  • Vasoconstrictors are also used clinically to
    increase blood pressure or to reduce local blood
    flow.

105
Epinephrine
  • Epinephrine stimulates alpha-, beta1-, and
    beta2-adrenergic receptors in dose-related
    fashion. It is the initial drug of choice for
    treating bronchoconstriction and hypotension
    resulting from anaphylaxis as well as all forms
    of cardiac arrest.

106
Epinephrine
  • It is useful in managing reactive airway disease,
    but beta-adrenergic agents are often used
    initially because of their convenience and oral
    inhalation route.
  • Rapid injection produces a rapid increase in
    systolic pressure, ventricular contractility, and
    heart rate.

107
Epinephrine
  • Epinephrine causes vasoconstriction in the
    arterioles of the skin, mucosa, and splanchnic
    areas and antagonizes the effects of histamine.
  • splanchnic nerves are part of the autonomic
    nervous system

108
Norepinephrine
  • Norepinephrine functions as a powerful peripheral
    vasoconstrictor (alpha-adrenergic action) and as
    a potent inotropic stimulator of the heart and
    dilator of coronary arteries (beta-adrenergic
    action).

109
Norepinephrine
  • Both of these actions result in an increase in
    systemic blood pressure and coronary artery blood
    flow.
  • Cardiac output will vary reflexly in response to
    systemic hypertension but is usually increased in
    hypotensive man when the blood pressure is raised
    to an optimal level.

110
Norepinephrine
  • In myocardial infarction accompanied by
    hypotension.
  • Norepinephrine usually increases aortic blood
    pressure, coronary artery blood flow, and
    myocardial oxygenation, thereby helping to limit
    the area of myocardial ischemia and infarction.
  • Venous return is increased and the heart tends to
    resume a more normal rate and rhythm than in the
    hypotensive state.

111
Dopamine
  • Dopamine as a medication acts on the sympathetic
    nervous system, producing effects such as
    increased heart rate and blood pressure.

112
Dopamine
  • It is a precursor to norepinephrine in
    noradrenergic nerves and is also a
    neurotransmitter in certain areas of
  • the central nervous system, especially
  • in the nigrostriatal tract, and in a few
    peripheral sympathetic nerves.

113
Dopamine
  • Dopamine produces positive chronotropic and
    inotropic effects on the myocardium, resulting in
    increased heart rate and cardiac contractility.
  • This is accomplished directly by exerting an
    agonist action on beta-adrenoceptors and
    indirectly by causing release of norepinephrine
    from storage sites in sympathetic nerve endings.

114
Dobutamine
  • Dobutamine is a beta adrenergic agonist. It acts
    on both beta-1 and beta-2 adrenergic receptors.

115
Dobutamine
  • Dobutamine increases myocardial contractility by
    stimulating ß1-adrenergic receptors in the heart,
    and causes vasodilation by stimulating
    ß2-adrenergic receptors in blood vessels,
    complemented by reflex vasodilation to the
    increase cardiac output.

116
Drugs used in the treatment of Shock
  • Vasodilators
  • Nipride (Sodium Nitroprusside)
  • Tridil (nitroglycerin)
  • Labetalol alpha-1 and non-selective beta blocker

117
Drugs used in the treatment of Shock
  • A vasodilator is a substance that causes blood
    vessels in the body to become wider by relaxing
    the smooth muscle in the vessel wall, or
    vasodilation.
  • This will reduce blood pressure (since there is
    more room for the blood) and might allow blood to
    flow around a clot. Several vasodilators are used
    as drugs.

118
Calcium Channel Blockers
  • Calcium channel blocking agents affect the
    movement of calcium into the cells of the heart
    and blood vessels. As a result, they relax blood
    vessels and increase the supply of blood and
    oxygen to the heart while reducing its workload.

119
Calcium Channel Blockers
  • Cardizem (diltiazem) drip, Ca channel blocker
  • Diltiazem is a member of the group of drugs known
    as calcium channel blockers, used in the
    treatment of hypertension or angina.
  • It is marketed under several brand names,
    including Cardizem, Cartia XT, and Tiazac.It is a
    class 3 anti anginal drug.it incites very minimal
    reflex sympathetic changes.

120
Calcium Channel Blockers
  • Verapamil Ca channel blocker
  • Verapamil (brand names Isoptin, Verelan,
    Calan) is a medical drug that acts as an L-type
    calcium channel blocker. It is used in the
    treatment of hypertension, angina pectoris, and
    some types of arrhythmia.

121
Volume expanders
  • If pt has a in the preload (intravascular volume
    depletion) give crystalloids to promote volume
    expansion. (Albumin, blood etc)
  • Mannitol ? restores intravascular volume

122
Vasoconstrictors
  • The vasoconstrictors are going to be used to
    afterload by increasing systemic vascular
    resistance
  • Vasodilators help to preload, systemic vascular
    resistance, venous return
  •  

123
Miscellaneous
  • Correct Lactacidosis induce hypoventilation
  • Na bicarbonate may help in acidosis
  • ( 7.1 pH). It might produce a rebound effect.
  • Nutritional Support
  • Initiate TPN in 24h or tube feeding

124
Post Test
125
Shock Syndromes
  • 1. True or False Regardless of the cause, Shock
    means inadequate tissue perfusion.

126
2.Match the pathophysiology with the type of
shock
  • 1.Vasodilation resulting from stimulation of the
    inflammatory and
  • immune systems by endotoxins
  • 2. Inability of heart to pump effectively.
  • 3. Vasodilation resulting from the release of
    histamine caused by major allergic reactions
  • 4. Vasodilation resulting from suppression or
    loss of sympathetic tone.

a. Cardiogenic b. Septic c. Anaphylactic d.
Neurogenic e. Hypovolemic
127
List three (3) types of Distributive Shock
  • 1.
  • 2.
  • 3.

128
Identify which type of shock the following
pathologic conditions or procedures may cause
129
Identify which type of shock the following
pathologic conditions or procedures may cause
130
Identify which type of shock the following
pathologic conditions or procedures may cause
131
Identify during which phase(s) of shock the
following clinical signs/symptoms are most likely
to occur
132
Identify during which phase(s) of shock the
following clinical signs/symptoms are most likely
to occur
133
Identify during which phase(s) of shock the
following clinical signs/symptoms are most likely
to occur
134
Identify during which phase(s) of shock the
following clinical signs/symptoms are most likely
to occur
135
For each type of shock, indicate if the following
hemodynamic parameters are increased, decreased,
or normal
136
(No Transcript)
137
For each the following types of shock list the
following treatment goal, pharmcologic
interventions, lab/diagnostic tests, restoration
of adequate tissue perfusion/oxygenation, pain
management and nutrition
138
  • True or false Diuretics are frequently used
    during fluid resuscitation of patients in shock
    due to fluid overload caused by overuse of
    colloids and crystalloids.

139
The End
140
References
  • Alspach, J. (1998).Core curriculum for critical
    care nursing(5th ed). American Association of
    Critical-Care Nurses.Philadelphia.Saunders.
  • Alspach, J. (1998).Core review for critical
    care nursing(5th ed). American Association of
    Critical-Care . Nurses. Philadelphia. Saunders.
  • Harvey, M. (1992). Core curriculum for critical
    care nursing. (2nd ed). American Association of
    Critical-Care . Philadelphia. Saunders.
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