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.