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The Physiology of ShockThe Physiology of Shock
R.E.B, 4MedStudents.com, 2003
• Shock occurs when
the rate of arterial blood flow is inadequate to meet
metabolic tissue needs and is the consequence of
cardio-vascular collapse
• Essentials of diagnosis are
– Hypotension (<60 mmHG)
– Tachycardia
– Oliguria
– Altered mental status
– Peripheral hypoperfusion and hypoxia
major types of shockmajor types of shock
• Hypovolemic shock
– Decreased intravascular volume resulting form loss of
blood, plasma, or fluids and electrolytes
• Cardiogenic shock
– Pump failure due to myocardial damage or massive
obstruction of outflow tracts
• Distributive shock
– Reduction of vascular resistance form
• Sepsis
• Anaphylaxis
• Systemic inflammatory response syndrome (SIRS)
• Hypovolemic shock
– Decreased intravascular volume resulting form loss of
blood, plasma, or fluids and electrolytes
• Cardiogenic shock
– Pump failure due to myocardial damage or massive
obstruction of outflow tracts
• Distributive shock
– Reduction of vascular resistance form
• Sepsis
• Anaphylaxis
• Systemic inflammatory response syndrome (SIRS)
Hypovolemic shock
(most common type of shock)
Hypovolemic shock
(most common type of shock)
• Loss of blood (hemorrhagic)
– External bleeding (wound to the outside or gastrointestinal)
– Internal bleeding (hematoma, hemothorax,
hemopertitoneum)
• Loss of plasma
– Burns
– Exfoliative dermatitis
• Loss of fluids and electrolytes
– External (vomiting, diarrhea, excessive sweating)
– Internal ( “third spacing” = pancreatitis, ascitis, bowl
obstruction
– Excessive sweating
Stages of hypovolemic shockStages of hypovolemic shock
• Mild (loss of < 20% blood volume)
– Few external signs in supine young patients but
• Increased capillary refill time ( longer 3 sec. = 10% volume loss)
• Moderate (loss of 20-40% blood volume)
– Patient becomes increasingly anxious and tachycardic >100 beats/min
(sympathetic response)
– oliguria
– blood pressure may be maintained in supine patient
• Severe (loss of > 40% blood volume)
– Classic signs of shock appear with hemodynamic instability
(Cave: if mental confusion occurs is an ominous clinical sign)
Only very short time frame may separate mild and severe shock
symptoms that lead, when left untreated, to progressive and
irreversible cell injury and death
• Mild (loss of < 20% blood volume)
– Few external signs in supine young patients but
• Increased capillary refill time ( longer 3 sec. = 10% volume loss)
• Moderate (loss of 20-40% blood volume)
– Patient becomes increasingly anxious and tachycardic >100 beats/min
(sympathetic response)
– oliguria
– blood pressure may be maintained in supine patient
• Severe (loss of > 40% blood volume)
– Classic signs of shock appear with hemodynamic instability
(Cave: if mental confusion occurs is an ominous clinical sign)
Only very short time frame may separate mild and severe shock
symptoms that lead, when left untreated, to progressive and
irreversible cell injury and death
Signs and Symptoms
• Low Blood Pressure
– Systolic BP is usually below 90 mmHg
• Pulse is rapid and weak
• Respiration is rapid and shallow
• Skin is pale, cool, and clammy
• Drowsiness
• Low Blood Pressure
– Systolic BP is usually below 90 mmHg
• Pulse is rapid and weak
• Respiration is rapid and shallow
• Skin is pale, cool, and clammy
• Drowsiness
Hypovolemic Shock
• Results from trauma in which there is blood
loss
• Decreased blood volume causes a decrease in
blood pressure
• Insufficient amounts of O2 is being transported
to body tissues and organs
Hypovolemic Shock
• Results from trauma in which there is blood
loss
• Decreased blood volume causes a decrease in
blood pressure
• Insufficient amounts of O2 is being transported
to body tissues and organs
Compensated Shock
• Early stages of shock where the body’s
compensatory mechanisms are able to
maintain normal perfusion
• Early stages of shock where the body’s
compensatory mechanisms are able to
maintain normal perfusion
Decompensated Shock
• Advanced stage of shock that occurs when the
body’s compensatory mechanisms fail to
maintain normal perfusion
• Advanced stage of shock that occurs when the
body’s compensatory mechanisms fail to
maintain normal perfusion
Irreversible Shock
• Stage of shock that has progressed to the point
that the body nor medical interventions correct
the problem
• Stage of shock that has progressed to the point
that the body nor medical interventions correct
the problem
Compensated and Decompensated
shock
• Usually the body is able to compensate but
when these mechanisms fail shock develops
and may progress
• Usually the body is able to compensate but
when these mechanisms fail shock develops
and may progress
Compensation Mechanisms
• Catecholamines may be secreted ( I.E.
Epinephrine and norepinephrine)
• The Renin-Angitensin system aids in
maintaining blood pressure
• Endocrine Response by pituitary gland results
in secretion of anti-diuretic hormone (ADH)
• Catecholamines may be secreted ( I.E.
Epinephrine and norepinephrine)
• The Renin-Angitensin system aids in
maintaining blood pressure
• Endocrine Response by pituitary gland results
in secretion of anti-diuretic hormone (ADH)
Catecholamine Release
• Epinephrine and Norepinephrine release
affects the cardiovascular system, causing
increase in HR, increase in Cardiac contractility
strength, arteriolar constriction which
elevates blood pressure
• Epinephrine and Norepinephrine release
affects the cardiovascular system, causing
increase in HR, increase in Cardiac contractility
strength, arteriolar constriction which
elevates blood pressure
Renin-Angiotensin system
• Renin is released from the kidneys and acts on
specialized plasma protein called
Angiotensinogen & produces Angiotensin I.
• Angiotensin I is converted to Angiotensin II by
enzymes in the lungs called Angiotensin
Converting Enzyme (ACE)
• Renin is released from the kidneys and acts on
specialized plasma protein called
Angiotensinogen & produces Angiotensin I.
• Angiotensin I is converted to Angiotensin II by
enzymes in the lungs called Angiotensin
Converting Enzyme (ACE)
Anti-Diuretic Hormone
• Causes the kidneys to reabsorb water creating
an additive to the aldostrone
• Causes the kidneys to reabsorb water creating
an additive to the aldostrone
Stages of ShockStages of Shock
• Initial non-progressive stage
– Baro-receptor reflexes
– Release of catecholamine
– Activation of renin-angiotensin-aldosteron system
– ADH release
results in tachycardia, peripheral vasoconstriction (cool skin) and renal fluid
conservation
• Progressive stage
– Widespread tissue hypoxia results in anaerobic glycolysis and
– Lactate acidosis (pH < 7.35)
– Vasodilation with blood pooling in microcirculation
– Declined cardiac output
– Oligouria
– Widespread tissue hypoxia
• Irreversible stage
– Widespread cell injury leading to
– Further decreased myocardial contractility
– Anuria with tubular necrosis
– Ischemic bowl may lead to leakage of bacterial flora
– Fluid in lung (ARDS)
S/S of Hypovolemic Shock
• Altered LOC
• Pale, cool, clammy skin
• Blood pressure may be normal then fall
• Pulse may be normal then become rapid, finally
slowing and disappearing
• Urination decreases
• Cardiac dysrhythmias may occur
• Altered LOC
• Pale, cool, clammy skin
• Blood pressure may be normal then fall
• Pulse may be normal then become rapid, finally
slowing and disappearing
• Urination decreases
• Cardiac dysrhythmias may occur
Tx for Hypovolemic Shock
• Airway control
• Administer high flow oxygen
• Control severe bleeding
• Keep patient warm
• Elevate lower extremities
• Establish IV and administer bolus of crystalloid
solution for fluid replacement
• Airway control
• Administer high flow oxygen
• Control severe bleeding
• Keep patient warm
• Elevate lower extremities
• Establish IV and administer bolus of crystalloid
solution for fluid replacement
Cardiogenic shockCardiogenic shock
• Pump failure
– Secondary to myocardial infarction (most common)
– Cardio-myophathy
– Acute valvular dysfunction (regurgitations)
– Rupture of the ventricular septum
• Arrhythmia
– Tachyarrhythmia
– Bradyarrhythmia
• Obstructions
– Tension pneumothorax
– Pericardial diseases (tamponade or constrictive pericarditis)
– Pulmonary hypertension (emboli or other vascular diseases)
Characteristics of Cardiogenic Shock
• Low cardiac output
• Peripheral vasoconstriction
• Left sided heart failure leads to pulmonary venous
congestion and pulmonary edema
• Right sided heart failure leads to systemic venous
congestion and peripheral edema
It is essential to distinguish a cardiogenic from a hypovolemic
shock!
Both forms are associated with reduced cardiac out put, and increased
peripheral vascular resistance, however:
It is essential to distinguish a cardiogenic from a hypovolemic
shock!
Both forms are associated with reduced cardiac out put, and increased
peripheral vascular resistance, however:
Cardiogenic shock:
jugular venous distention (high CVP)
Hypovolemic shock: collapsed
capacitance veins (low CVP)
Cardiogenic shock:
jugular venous distention (high CVP)
Hypovolemic shock: collapsed
capacitance veins (low CVP)
Cardiogenic Shock
• The heart loses the ability to supply all body
parts with blood
• Usually the result of left ventricular failure
secondary to acute MI or CHF
• Many patients will have normal blood
pressures
• The heart loses the ability to supply all body
parts with blood
• Usually the result of left ventricular failure
secondary to acute MI or CHF
• Many patients will have normal blood
pressures
S/S of Cardiogenic Shock
• Major difference between other types of shock
is presence of Pulmonary Edema
• Difficulty breathing
• Wheezes, Crackles, Rales are heard as fluid
levels increase
• Productive cough with white or pink-tinged
foamy sputum
• Cyanosis
• Altered mentation
• Oliguria ( decreased urination)
• Major difference between other types of shock
is presence of Pulmonary Edema
• Difficulty breathing
• Wheezes, Crackles, Rales are heard as fluid
levels increase
• Productive cough with white or pink-tinged
foamy sputum
• Cyanosis
• Altered mentation
• Oliguria ( decreased urination)
TX for Cardiogenic Shock
• Assure open airway
• Adminster oxygen
• Assist ventilations as needed
• Keep patient warm
• Place patient in position of comfort
• Establish Iv with minimal fluid administration
• Monitor Vitals
• May need to administer Dopamine or
Dobutamine
• Assure open airway
• Adminster oxygen
• Assist ventilations as needed
• Keep patient warm
• Place patient in position of comfort
• Establish Iv with minimal fluid administration
• Monitor Vitals
• May need to administer Dopamine or
Dobutamine
Distributive ShockDistributive Shock
• Sepsis
– Due to gram negative or gram positive bacteria
• Anaphylaxis
– Due to previous sensitization to an allergen
• Neurogenic
– Due to traumatic spinal cord injury
– Effects of epidural or spinal anesthetics
– Reflex parasymapthetic stimulation
• Sepsis
– Due to gram negative or gram positive bacteria
• Anaphylaxis
– Due to previous sensitization to an allergen
• Neurogenic
– Due to traumatic spinal cord injury
– Effects of epidural or spinal anesthetics
– Reflex parasymapthetic stimulation
Types of ShockTypes of Shock
Neurogenic Shock
• Results due to the overall dilation of the blood
vessels within the cardiovascular system
• Decreased blood pressure
• Insufficient amounts of O2 is being transported
to body tissues and organs
Neurogenic Shock
• Results due to the overall dilation of the blood
vessels within the cardiovascular system
• Decreased blood pressure
• Insufficient amounts of O2 is being transported
to body tissues and organs
Neurogenic Shock
• Results from injury to brain or spinal cord
causing interruption of nerve impulses to
arteries
• Arteries lose tone and dilate causing
hypovolemia
• Sympathetic nerve impulses to the adrenal
glands are lost, which prevents the release of
catecholamines and their compensatory effects
• Results from injury to brain or spinal cord
causing interruption of nerve impulses to
arteries
• Arteries lose tone and dilate causing
hypovolemia
• Sympathetic nerve impulses to the adrenal
glands are lost, which prevents the release of
catecholamines and their compensatory effects
Neurogenic Shock (con’t)
• High cervical injuries cause interruption of
impulse to peripheral nervous system causing
• Neurogenic shock is most commonly due to
severe injury to spinal cord or total transection
of cord (spinal shock)
• High cervical injuries cause interruption of
impulse to peripheral nervous system causing
• Neurogenic shock is most commonly due to
severe injury to spinal cord or total transection
of cord (spinal shock)
S/S of Neurogenic Shock
• Warm, Dry, Red Skin
• Low Blood Pressure
• Slow Pulse
• Warm, Dry, Red Skin
• Low Blood Pressure
• Slow Pulse
TX for Neurogenic Shock
• Airway control
• Maintain body temperature
• Immobilization if indicated
• Consider other causes of shock
• IV and medications that increase peripheral
vascular resistance (I.E. Norepinephrine,
Dopamine)
• Airway control
• Maintain body temperature
• Immobilization if indicated
• Consider other causes of shock
• IV and medications that increase peripheral
vascular resistance (I.E. Norepinephrine,
Dopamine)
Anaphylatic Shock
• Severe immune response to foreign substance
• S/S most often occur within minutes but can
take up to hours to occur
• The faster the reaction develops the more
severe it is likely to be
• Death will occur if not treated promptly
• Severe immune response to foreign substance
• S/S most often occur within minutes but can
take up to hours to occur
• The faster the reaction develops the more
severe it is likely to be
• Death will occur if not treated promptly
S/S of Anaphylactic Shock
• Skin
- Flushing
- Itching
- Hives
-Swelling
-Cyanosis
• Skin
- Flushing
- Itching
- Hives
-Swelling
-Cyanosis
S/S of Anaphylactic Shock
• Respiratory System
- Breathing difficulty
- Sneezing, Coughing
- Wheezing, Stridor
- Laryngeal edema
- Laryngospasm
• Respiratory System
- Breathing difficulty
- Sneezing, Coughing
- Wheezing, Stridor
- Laryngeal edema
- Laryngospasm
S/S of Anaphylactic Shock
• Cardiovascular System
- Vasodilation
- Increased heart rate
- Decreased blood pressure
• Cardiovascular System
- Vasodilation
- Increased heart rate
- Decreased blood pressure
S/S of Anaphylactic Shock
• Gastrointestinal System
- Nausea, vomiting
- Abdominal cramping
- Diarrhea
• Gastrointestinal System
- Nausea, vomiting
- Abdominal cramping
- Diarrhea
TX for Anaphylactic Shock
• Airway protection which may include
Endotracheal Intubation
• Establish IV with crystalloid solution
• Pharmacological interventions: Epinephrine,
Antihistamines(Benadryl),
Corticosteroids(dexamethasone),
Vasopressors(dopamine, Epinephrine), and
inhaled beta agonist(albuterol)
• Airway protection which may include
Endotracheal Intubation
• Establish IV with crystalloid solution
• Pharmacological interventions: Epinephrine,
Antihistamines(Benadryl),
Corticosteroids(dexamethasone),
Vasopressors(dopamine, Epinephrine), and
inhaled beta agonist(albuterol)
Pathogenesis of Septic Shock
(vasodilatory shock)
• Sepsis is defined as a systemic inflammatory response
to a bacterial infection with bacteriemia (though
blood cultures can be negative)
• Severe sepsis is defined by additional end-organ
dysfunction (mortality rate: 25-30%)
• Septic shock is defined as sepsis with hypotension
despite fluid resuscitation and evidence of inadequate
tissue perfusion (40-70%)
• Sepsis is defined as a systemic inflammatory response
to a bacterial infection with bacteriemia (though
blood cultures can be negative)
• Severe sepsis is defined by additional end-organ
dysfunction (mortality rate: 25-30%)
• Septic shock is defined as sepsis with hypotension
despite fluid resuscitation and evidence of inadequate
tissue perfusion (40-70%)
NEJM 2004, Vol. 351;2 pp 159-169
Clinical Spectrum of Infection
Infection
Sepsis
Severe Sepsis
Septic Shock
Bacteremia
The syndrome of septic shock is characterized
by
• Systemic vasodilation (hypotension)
• Diminished myocardial contractility
• Widespread endothelial injury and activation leading
to fluid leakage (capillary leak) resulting in acute
respiratory distress syndrome (ARDS)
• Activation of the coagulation cascade (DIC)
• Systemic vasodilation (hypotension)
• Diminished myocardial contractility
• Widespread endothelial injury and activation leading
to fluid leakage (capillary leak) resulting in acute
respiratory distress syndrome (ARDS)
• Activation of the coagulation cascade (DIC)
Disseminated intravascular coagulation (DIC)
• is characterized by widespread activation of coagulation
resulting in the intravascular formation of fibrin and ultimately
thrombotic occlusion of small and midsize vessels
• leads to compromise of blood supply to organs and may
therefore contribute to multiple organ failure
• subsequent depletion of platelets and coagulation factors can
result in severe bleeding and may be the presenting symptom
• is characterized by widespread activation of coagulation
resulting in the intravascular formation of fibrin and ultimately
thrombotic occlusion of small and midsize vessels
• leads to compromise of blood supply to organs and may
therefore contribute to multiple organ failure
• subsequent depletion of platelets and coagulation factors can
result in severe bleeding and may be the presenting symptom
Virtually all patients with sepsis have coagulation
abnormalities. The extreme form of it is called:
Acute disseminated intravascular coagulation (DIC)
Severe cutaneous bleeding as a result of fulminant Meningococcal
septicemia due to activation and consumption of all coagulation
factors (consumption coagulopathy)
Septic Shock
• An infection enters bloodstream and is carried
throughout body
• Toxins released overcome compensatory
mechanisms
• Can cause dysfunction of one organ system or
cause multiple organ dysfunction
• An infection enters bloodstream and is carried
throughout body
• Toxins released overcome compensatory
mechanisms
• Can cause dysfunction of one organ system or
cause multiple organ dysfunction
S/S of Septic Shock
• Increased to low blood pressure
• High fever, no fever, hypothermic
• Skin flushed, Pale, Cyanotic
• Difficulty breathing and altered lung sounds
• Altered LOC
• Increased to low blood pressure
• High fever, no fever, hypothermic
• Skin flushed, Pale, Cyanotic
• Difficulty breathing and altered lung sounds
• Altered LOC
TX of Septic Shock
• Airway control
• Administer oxygen
• IV of crystalloid solution
• Dopamine for blood pressure support
• Monitor other vitals
• Airway control
• Administer oxygen
• IV of crystalloid solution
• Dopamine for blood pressure support
• Monitor other vitals
Physiology of  shock
Physiology of  shock

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Physiology of shock

  • 1.
  • 2. 2 The Physiology of ShockThe Physiology of Shock R.E.B, 4MedStudents.com, 2003
  • 3.
  • 4. • Shock occurs when the rate of arterial blood flow is inadequate to meet metabolic tissue needs and is the consequence of cardio-vascular collapse • Essentials of diagnosis are – Hypotension (<60 mmHG) – Tachycardia – Oliguria – Altered mental status – Peripheral hypoperfusion and hypoxia
  • 5.
  • 6. major types of shockmajor types of shock • Hypovolemic shock – Decreased intravascular volume resulting form loss of blood, plasma, or fluids and electrolytes • Cardiogenic shock – Pump failure due to myocardial damage or massive obstruction of outflow tracts • Distributive shock – Reduction of vascular resistance form • Sepsis • Anaphylaxis • Systemic inflammatory response syndrome (SIRS) • Hypovolemic shock – Decreased intravascular volume resulting form loss of blood, plasma, or fluids and electrolytes • Cardiogenic shock – Pump failure due to myocardial damage or massive obstruction of outflow tracts • Distributive shock – Reduction of vascular resistance form • Sepsis • Anaphylaxis • Systemic inflammatory response syndrome (SIRS)
  • 7. Hypovolemic shock (most common type of shock) Hypovolemic shock (most common type of shock) • Loss of blood (hemorrhagic) – External bleeding (wound to the outside or gastrointestinal) – Internal bleeding (hematoma, hemothorax, hemopertitoneum) • Loss of plasma – Burns – Exfoliative dermatitis • Loss of fluids and electrolytes – External (vomiting, diarrhea, excessive sweating) – Internal ( “third spacing” = pancreatitis, ascitis, bowl obstruction – Excessive sweating
  • 8. Stages of hypovolemic shockStages of hypovolemic shock • Mild (loss of < 20% blood volume) – Few external signs in supine young patients but • Increased capillary refill time ( longer 3 sec. = 10% volume loss) • Moderate (loss of 20-40% blood volume) – Patient becomes increasingly anxious and tachycardic >100 beats/min (sympathetic response) – oliguria – blood pressure may be maintained in supine patient • Severe (loss of > 40% blood volume) – Classic signs of shock appear with hemodynamic instability (Cave: if mental confusion occurs is an ominous clinical sign) Only very short time frame may separate mild and severe shock symptoms that lead, when left untreated, to progressive and irreversible cell injury and death • Mild (loss of < 20% blood volume) – Few external signs in supine young patients but • Increased capillary refill time ( longer 3 sec. = 10% volume loss) • Moderate (loss of 20-40% blood volume) – Patient becomes increasingly anxious and tachycardic >100 beats/min (sympathetic response) – oliguria – blood pressure may be maintained in supine patient • Severe (loss of > 40% blood volume) – Classic signs of shock appear with hemodynamic instability (Cave: if mental confusion occurs is an ominous clinical sign) Only very short time frame may separate mild and severe shock symptoms that lead, when left untreated, to progressive and irreversible cell injury and death
  • 9. Signs and Symptoms • Low Blood Pressure – Systolic BP is usually below 90 mmHg • Pulse is rapid and weak • Respiration is rapid and shallow • Skin is pale, cool, and clammy • Drowsiness • Low Blood Pressure – Systolic BP is usually below 90 mmHg • Pulse is rapid and weak • Respiration is rapid and shallow • Skin is pale, cool, and clammy • Drowsiness
  • 10. Hypovolemic Shock • Results from trauma in which there is blood loss • Decreased blood volume causes a decrease in blood pressure • Insufficient amounts of O2 is being transported to body tissues and organs Hypovolemic Shock • Results from trauma in which there is blood loss • Decreased blood volume causes a decrease in blood pressure • Insufficient amounts of O2 is being transported to body tissues and organs
  • 11.
  • 12.
  • 13. Compensated Shock • Early stages of shock where the body’s compensatory mechanisms are able to maintain normal perfusion • Early stages of shock where the body’s compensatory mechanisms are able to maintain normal perfusion
  • 14. Decompensated Shock • Advanced stage of shock that occurs when the body’s compensatory mechanisms fail to maintain normal perfusion • Advanced stage of shock that occurs when the body’s compensatory mechanisms fail to maintain normal perfusion
  • 15. Irreversible Shock • Stage of shock that has progressed to the point that the body nor medical interventions correct the problem • Stage of shock that has progressed to the point that the body nor medical interventions correct the problem
  • 16.
  • 17.
  • 18.
  • 19.
  • 20.
  • 21.
  • 22. Compensated and Decompensated shock • Usually the body is able to compensate but when these mechanisms fail shock develops and may progress • Usually the body is able to compensate but when these mechanisms fail shock develops and may progress
  • 23. Compensation Mechanisms • Catecholamines may be secreted ( I.E. Epinephrine and norepinephrine) • The Renin-Angitensin system aids in maintaining blood pressure • Endocrine Response by pituitary gland results in secretion of anti-diuretic hormone (ADH) • Catecholamines may be secreted ( I.E. Epinephrine and norepinephrine) • The Renin-Angitensin system aids in maintaining blood pressure • Endocrine Response by pituitary gland results in secretion of anti-diuretic hormone (ADH)
  • 24. Catecholamine Release • Epinephrine and Norepinephrine release affects the cardiovascular system, causing increase in HR, increase in Cardiac contractility strength, arteriolar constriction which elevates blood pressure • Epinephrine and Norepinephrine release affects the cardiovascular system, causing increase in HR, increase in Cardiac contractility strength, arteriolar constriction which elevates blood pressure
  • 25. Renin-Angiotensin system • Renin is released from the kidneys and acts on specialized plasma protein called Angiotensinogen & produces Angiotensin I. • Angiotensin I is converted to Angiotensin II by enzymes in the lungs called Angiotensin Converting Enzyme (ACE) • Renin is released from the kidneys and acts on specialized plasma protein called Angiotensinogen & produces Angiotensin I. • Angiotensin I is converted to Angiotensin II by enzymes in the lungs called Angiotensin Converting Enzyme (ACE)
  • 26. Anti-Diuretic Hormone • Causes the kidneys to reabsorb water creating an additive to the aldostrone • Causes the kidneys to reabsorb water creating an additive to the aldostrone
  • 27. Stages of ShockStages of Shock • Initial non-progressive stage – Baro-receptor reflexes – Release of catecholamine – Activation of renin-angiotensin-aldosteron system – ADH release results in tachycardia, peripheral vasoconstriction (cool skin) and renal fluid conservation • Progressive stage – Widespread tissue hypoxia results in anaerobic glycolysis and – Lactate acidosis (pH < 7.35) – Vasodilation with blood pooling in microcirculation – Declined cardiac output – Oligouria – Widespread tissue hypoxia • Irreversible stage – Widespread cell injury leading to – Further decreased myocardial contractility – Anuria with tubular necrosis – Ischemic bowl may lead to leakage of bacterial flora – Fluid in lung (ARDS)
  • 28.
  • 29.
  • 30.
  • 31.
  • 32. S/S of Hypovolemic Shock • Altered LOC • Pale, cool, clammy skin • Blood pressure may be normal then fall • Pulse may be normal then become rapid, finally slowing and disappearing • Urination decreases • Cardiac dysrhythmias may occur • Altered LOC • Pale, cool, clammy skin • Blood pressure may be normal then fall • Pulse may be normal then become rapid, finally slowing and disappearing • Urination decreases • Cardiac dysrhythmias may occur
  • 33. Tx for Hypovolemic Shock • Airway control • Administer high flow oxygen • Control severe bleeding • Keep patient warm • Elevate lower extremities • Establish IV and administer bolus of crystalloid solution for fluid replacement • Airway control • Administer high flow oxygen • Control severe bleeding • Keep patient warm • Elevate lower extremities • Establish IV and administer bolus of crystalloid solution for fluid replacement
  • 34.
  • 35.
  • 36. Cardiogenic shockCardiogenic shock • Pump failure – Secondary to myocardial infarction (most common) – Cardio-myophathy – Acute valvular dysfunction (regurgitations) – Rupture of the ventricular septum • Arrhythmia – Tachyarrhythmia – Bradyarrhythmia • Obstructions – Tension pneumothorax – Pericardial diseases (tamponade or constrictive pericarditis) – Pulmonary hypertension (emboli or other vascular diseases)
  • 37. Characteristics of Cardiogenic Shock • Low cardiac output • Peripheral vasoconstriction • Left sided heart failure leads to pulmonary venous congestion and pulmonary edema • Right sided heart failure leads to systemic venous congestion and peripheral edema
  • 38. It is essential to distinguish a cardiogenic from a hypovolemic shock! Both forms are associated with reduced cardiac out put, and increased peripheral vascular resistance, however: It is essential to distinguish a cardiogenic from a hypovolemic shock! Both forms are associated with reduced cardiac out put, and increased peripheral vascular resistance, however: Cardiogenic shock: jugular venous distention (high CVP) Hypovolemic shock: collapsed capacitance veins (low CVP) Cardiogenic shock: jugular venous distention (high CVP) Hypovolemic shock: collapsed capacitance veins (low CVP)
  • 39. Cardiogenic Shock • The heart loses the ability to supply all body parts with blood • Usually the result of left ventricular failure secondary to acute MI or CHF • Many patients will have normal blood pressures • The heart loses the ability to supply all body parts with blood • Usually the result of left ventricular failure secondary to acute MI or CHF • Many patients will have normal blood pressures
  • 40. S/S of Cardiogenic Shock • Major difference between other types of shock is presence of Pulmonary Edema • Difficulty breathing • Wheezes, Crackles, Rales are heard as fluid levels increase • Productive cough with white or pink-tinged foamy sputum • Cyanosis • Altered mentation • Oliguria ( decreased urination) • Major difference between other types of shock is presence of Pulmonary Edema • Difficulty breathing • Wheezes, Crackles, Rales are heard as fluid levels increase • Productive cough with white or pink-tinged foamy sputum • Cyanosis • Altered mentation • Oliguria ( decreased urination)
  • 41. TX for Cardiogenic Shock • Assure open airway • Adminster oxygen • Assist ventilations as needed • Keep patient warm • Place patient in position of comfort • Establish Iv with minimal fluid administration • Monitor Vitals • May need to administer Dopamine or Dobutamine • Assure open airway • Adminster oxygen • Assist ventilations as needed • Keep patient warm • Place patient in position of comfort • Establish Iv with minimal fluid administration • Monitor Vitals • May need to administer Dopamine or Dobutamine
  • 42. Distributive ShockDistributive Shock • Sepsis – Due to gram negative or gram positive bacteria • Anaphylaxis – Due to previous sensitization to an allergen • Neurogenic – Due to traumatic spinal cord injury – Effects of epidural or spinal anesthetics – Reflex parasymapthetic stimulation • Sepsis – Due to gram negative or gram positive bacteria • Anaphylaxis – Due to previous sensitization to an allergen • Neurogenic – Due to traumatic spinal cord injury – Effects of epidural or spinal anesthetics – Reflex parasymapthetic stimulation
  • 43. Types of ShockTypes of Shock Neurogenic Shock • Results due to the overall dilation of the blood vessels within the cardiovascular system • Decreased blood pressure • Insufficient amounts of O2 is being transported to body tissues and organs Neurogenic Shock • Results due to the overall dilation of the blood vessels within the cardiovascular system • Decreased blood pressure • Insufficient amounts of O2 is being transported to body tissues and organs
  • 44.
  • 45.
  • 46. Neurogenic Shock • Results from injury to brain or spinal cord causing interruption of nerve impulses to arteries • Arteries lose tone and dilate causing hypovolemia • Sympathetic nerve impulses to the adrenal glands are lost, which prevents the release of catecholamines and their compensatory effects • Results from injury to brain or spinal cord causing interruption of nerve impulses to arteries • Arteries lose tone and dilate causing hypovolemia • Sympathetic nerve impulses to the adrenal glands are lost, which prevents the release of catecholamines and their compensatory effects
  • 47. Neurogenic Shock (con’t) • High cervical injuries cause interruption of impulse to peripheral nervous system causing • Neurogenic shock is most commonly due to severe injury to spinal cord or total transection of cord (spinal shock) • High cervical injuries cause interruption of impulse to peripheral nervous system causing • Neurogenic shock is most commonly due to severe injury to spinal cord or total transection of cord (spinal shock)
  • 48. S/S of Neurogenic Shock • Warm, Dry, Red Skin • Low Blood Pressure • Slow Pulse • Warm, Dry, Red Skin • Low Blood Pressure • Slow Pulse
  • 49. TX for Neurogenic Shock • Airway control • Maintain body temperature • Immobilization if indicated • Consider other causes of shock • IV and medications that increase peripheral vascular resistance (I.E. Norepinephrine, Dopamine) • Airway control • Maintain body temperature • Immobilization if indicated • Consider other causes of shock • IV and medications that increase peripheral vascular resistance (I.E. Norepinephrine, Dopamine)
  • 50.
  • 51.
  • 52. Anaphylatic Shock • Severe immune response to foreign substance • S/S most often occur within minutes but can take up to hours to occur • The faster the reaction develops the more severe it is likely to be • Death will occur if not treated promptly • Severe immune response to foreign substance • S/S most often occur within minutes but can take up to hours to occur • The faster the reaction develops the more severe it is likely to be • Death will occur if not treated promptly
  • 53.
  • 54. S/S of Anaphylactic Shock • Skin - Flushing - Itching - Hives -Swelling -Cyanosis • Skin - Flushing - Itching - Hives -Swelling -Cyanosis
  • 55. S/S of Anaphylactic Shock • Respiratory System - Breathing difficulty - Sneezing, Coughing - Wheezing, Stridor - Laryngeal edema - Laryngospasm • Respiratory System - Breathing difficulty - Sneezing, Coughing - Wheezing, Stridor - Laryngeal edema - Laryngospasm
  • 56. S/S of Anaphylactic Shock • Cardiovascular System - Vasodilation - Increased heart rate - Decreased blood pressure • Cardiovascular System - Vasodilation - Increased heart rate - Decreased blood pressure
  • 57. S/S of Anaphylactic Shock • Gastrointestinal System - Nausea, vomiting - Abdominal cramping - Diarrhea • Gastrointestinal System - Nausea, vomiting - Abdominal cramping - Diarrhea
  • 58. TX for Anaphylactic Shock • Airway protection which may include Endotracheal Intubation • Establish IV with crystalloid solution • Pharmacological interventions: Epinephrine, Antihistamines(Benadryl), Corticosteroids(dexamethasone), Vasopressors(dopamine, Epinephrine), and inhaled beta agonist(albuterol) • Airway protection which may include Endotracheal Intubation • Establish IV with crystalloid solution • Pharmacological interventions: Epinephrine, Antihistamines(Benadryl), Corticosteroids(dexamethasone), Vasopressors(dopamine, Epinephrine), and inhaled beta agonist(albuterol)
  • 59.
  • 60.
  • 61. Pathogenesis of Septic Shock (vasodilatory shock) • Sepsis is defined as a systemic inflammatory response to a bacterial infection with bacteriemia (though blood cultures can be negative) • Severe sepsis is defined by additional end-organ dysfunction (mortality rate: 25-30%) • Septic shock is defined as sepsis with hypotension despite fluid resuscitation and evidence of inadequate tissue perfusion (40-70%) • Sepsis is defined as a systemic inflammatory response to a bacterial infection with bacteriemia (though blood cultures can be negative) • Severe sepsis is defined by additional end-organ dysfunction (mortality rate: 25-30%) • Septic shock is defined as sepsis with hypotension despite fluid resuscitation and evidence of inadequate tissue perfusion (40-70%)
  • 62.
  • 63. NEJM 2004, Vol. 351;2 pp 159-169
  • 64. Clinical Spectrum of Infection Infection Sepsis Severe Sepsis Septic Shock Bacteremia
  • 65.
  • 66. The syndrome of septic shock is characterized by • Systemic vasodilation (hypotension) • Diminished myocardial contractility • Widespread endothelial injury and activation leading to fluid leakage (capillary leak) resulting in acute respiratory distress syndrome (ARDS) • Activation of the coagulation cascade (DIC) • Systemic vasodilation (hypotension) • Diminished myocardial contractility • Widespread endothelial injury and activation leading to fluid leakage (capillary leak) resulting in acute respiratory distress syndrome (ARDS) • Activation of the coagulation cascade (DIC)
  • 67.
  • 68. Disseminated intravascular coagulation (DIC) • is characterized by widespread activation of coagulation resulting in the intravascular formation of fibrin and ultimately thrombotic occlusion of small and midsize vessels • leads to compromise of blood supply to organs and may therefore contribute to multiple organ failure • subsequent depletion of platelets and coagulation factors can result in severe bleeding and may be the presenting symptom • is characterized by widespread activation of coagulation resulting in the intravascular formation of fibrin and ultimately thrombotic occlusion of small and midsize vessels • leads to compromise of blood supply to organs and may therefore contribute to multiple organ failure • subsequent depletion of platelets and coagulation factors can result in severe bleeding and may be the presenting symptom
  • 69. Virtually all patients with sepsis have coagulation abnormalities. The extreme form of it is called: Acute disseminated intravascular coagulation (DIC) Severe cutaneous bleeding as a result of fulminant Meningococcal septicemia due to activation and consumption of all coagulation factors (consumption coagulopathy)
  • 70.
  • 71. Septic Shock • An infection enters bloodstream and is carried throughout body • Toxins released overcome compensatory mechanisms • Can cause dysfunction of one organ system or cause multiple organ dysfunction • An infection enters bloodstream and is carried throughout body • Toxins released overcome compensatory mechanisms • Can cause dysfunction of one organ system or cause multiple organ dysfunction
  • 72. S/S of Septic Shock • Increased to low blood pressure • High fever, no fever, hypothermic • Skin flushed, Pale, Cyanotic • Difficulty breathing and altered lung sounds • Altered LOC • Increased to low blood pressure • High fever, no fever, hypothermic • Skin flushed, Pale, Cyanotic • Difficulty breathing and altered lung sounds • Altered LOC
  • 73. TX of Septic Shock • Airway control • Administer oxygen • IV of crystalloid solution • Dopamine for blood pressure support • Monitor other vitals • Airway control • Administer oxygen • IV of crystalloid solution • Dopamine for blood pressure support • Monitor other vitals

Editor's Notes

  1. Septic shock is a continuumalong this pathway of worsening of microorganisms in normally sterile host tissues and their ongoing invasion. Infection- the presence of microorganisms in normally sterile host tissue. Bacteremia- the presence of viable bacteria in blood Sepsis- The systemic response to infection Severe sepsis- sepsis associated with organ dysfunction, hypoperfusion or hypotension. Septic shock- sepsis with hypotension despite adequate fluid resuscitation, and perfusion abnormalitites. 71% of patients with culture proven septic shock are initially identified as being in one of the milder categories, yet only 4% of patients with SIRS progress to full septick shock. Rangel-Fausto MS, Pittet D, Castigan M, Hwang T, et al., The natural history of the systemic inflammatory response syndrome. JAMA 1995; 273: 117-123. Its important to identify these patients early when they are more amenable to succsessful intervention.