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Pathology and Pathophysiology of Shock
Marc Imhotep Cray M.D.
Marc Imhotep Cray, M.D.
Learning Objectives
2
1. Discuss the general concepts associated with shock states,
including physiologic response to shock, and shock
progression.
2. Describe cardiogenic shock, including pathophysiology,
clinical manifestations, diagnosis, and management.
3. Discuss hypovolemic shock, including pathophysiology,
clinical manifestations, diagnosis, and management.
4. Explain the septic type of distributive shock, including
pathophysiology, clinical manifestations, diagnosis, and
management.
By the end of this lecture the learner should be able to:
Marc Imhotep Cray, M.D.
Learning Objectives
3
5. Discuss the neurologic and anaphylactic types of
distributive shock, including the pathophysiology, clinical
manifestations, diagnosis, and management of each type.
6. Describe the major causes of obstructive shock, including
the pathophysiology, clinical manifestations, diagnosis, and
management of each cause
7. Discuss use of pharmacotherapy in the management of
shock states.
By the end of this lecture the learner should be able to:
Marc Imhotep Cray, M.D.
Shock Capsule
4
 Shock is a clinical condition characterized by a fast pulse rate
(usually > 100 beats/min) and a low blood pressure (systolic
blood pressure usually < 100 mmHg)
 Common types of shock are
 hypovolemic (low blood volume, e.g. in hemorrhage),
 cardiogenic (heart pump failure, e.g. in myocardial infarction)
 septic (severe infection)
 Less common types are
 anaphylactic (type I hypersensitivity reaction, e.g. penicillin
allergy)
 neurogenic (loss of sympathetic vasomotor tone, e.g. in a
spinal cord injury)
Marc Imhotep Cray, M.D.
Shock, Pathology of Different Types,
Animation_Alila Medical Media
5Online Version
Marc Imhotep Cray, M.D.
Stages of Shock
6
As stated above Shock is a progressive disorder that
leads to death if underlying causes are not corrected
 Exact mechanisms of sepsis-related death are still unclear;
aside from increased lymphocyte and enterocyte apoptosis,
cellular necrosis is minimal
• Death typically follows the failure of multiple organs usually offer no
morphological clues to explain their dysfunction
 For hypovolemic and cardiogenic shock pathways leading to a
patient’s demise are reasonably well understood tissue ischemia,
acute tubular necrosis, lactic acidosis severe cellular and tissue
injury cardiopulmonary arrest
 Unless insult is massive and rapidly lethal (e.g., exsanguination
from a ruptured aortic aneurysm), shock tends to evolve through
three general (albeit somewhat artificial) stages…
Marc Imhotep Cray, M.D.
The 3 Stages of Shock
7
These stages have been documented most clearly in
hypovolemic shock but are common to other forms as well:
 Stage 1 An initial nonprogressive stage during which reflex
compensatory mechanisms are activated and vital organ perfusion
is maintained
 Stage 2 A progressive stage characterized by tissue hypoperfusion
and onset of worsening circulatory and metabolic derangement,
including acidosis
 Stage 3 An irreversible stage in which cellular and tissue injury is so
severe that even if hemodynamic defects are corrected, survival is
not possible
Marc Imhotep Cray, M.D.
Shock, Circulatory Defined
8
Circulatory shock, commonly known as just shock, is a serious, life-
threatening medical condition where insufficient blood flow
reaches body tissues
 As blood carries oxygen and nutrients around body, reduced flow
hinders delivery of these components to tissues, and can stop
tissues from functioning properly
The process of blood entering tissues is called perfusion, so when
perfusion is not occurring properly this is called a hypoperfusional
(hypo = below) state
Marc Imhotep Cray, M.D.
Shock (circulatory)
9
Effects of inadequate perfusion on cell function
Learn more from Dr. Najeeb’s Video Series on Circulatory shock
Marc Imhotep Cray, M.D.
The problem in shock
10
From: http://www.cvpharmacology.com/clinical
topics/hypotension.htm
• Altered circulatory
parameters
• Compromised
microcirculation
• Persistent severe
hypoxia
• Multiple organ failure
Marc Imhotep Cray, M.D.
Main Types of Shock
11
Vasoconstrictive
• Trauma, bleeding, burning, ileus (volumen loss)
• Pulmonary embolism (impaired cardiac filling)
• Myocardial infarction (impaired cardiac contraction)
Vasodilatative
• Anaphylaxis, sepsis (maldistribution of blood flow)
• Spinal medullary injury (venous pooling)
• Hypothermia
Marc Imhotep Cray, M.D.
Classification of Shock
12
• In 1972 Hinshaw and Cox suggested following
classification which is still used today
• It uses four types of shock:
1. hypovolemic
2. cardiogenic
3. distributive and
4. obstructive shock
Marc Imhotep Cray, M.D.
Classification
(Based on cardiovascular characteristics, which was initially proposed
in 1972 by Hinshaw and Cox.)
13
Hypovolemic
Hemorrhagic
Fluid depletion
Increased vascular capacitance
Cardiogenic
Myopathic
Mechanical
Arrhythmic
Distributive
Septic, etc.
Obstructive
PE, pericarditis, pnumothorax etc.
Marc Imhotep Cray, M.D.
Hypovolemic shock
14
Hypovolemic shock
This is most common type of shock and based on insufficient
circulating volume = circulating shock
• Its primary cause is loss of fluid from circulation from either an
internal or external source
• An internal source may be hemorrhage
• External causes may include extensive bleeding, high output
fistulae (greater than 500 ml per day)or severe burns
Marc Imhotep Cray, M.D.
Hypovolemic Shock
15
Low central venous pressure (CVP), Low pulmonary capillary wedge
pressure (PCWP), Low cardiac output (CO) and cardiac index (CI), and high
SVR arterial blood pressure may be normal or low
Loss in circulatory volume
• Decreased venous return
• Decreased filling of cardiac chambers
• Decreased cardiac output
• increase in systemic vascular resistance (SVR)
Marc Imhotep Cray, M.D.
Hypovolemic Shock (2) Causes
16
Hemorrhagic
• Trauma
• Gastrointestinal
• Retroperitoneal
Fluid depletion
(nonhemorrhagic)
• External fluid loss
• Dehydration
• Vomiting
• Diarrhea
• Polyuria
Interstitial fluid redistribution
• Thermal injury
• Trauma
• Anaphylaxis
Increased vascular capacitance
(venodilation)
• Sepsis
• Anaphylaxis
• Toxins/Drugs
Marc Imhotep Cray, M.D.
Cardiogenic shock
17
Cardiogenic shock
This type of shock is caused by failure of heart to pump
effectively
• This can be due to damage to heart muscle, most often
from a large myocardial infarction
• Other causes of cardiogenic shock include
o arrhythmias,
o cardiomyopathy,
o congestive heart failure (CHF), and
o cardiac valve problems
Marc Imhotep Cray, M.D.
Cardiogenic Shock (2)
18
• dependent on poor pump function
• acute catastrophic failure of LV pump function
High PCWP, low CO and CI, and generally a high SVR
Marc Imhotep Cray, M.D.
Cardiogenic (3)
19
Myopathic
• Myocardial infarction (left ventricle, right ventricle)
• Elevations in CK-MB and Troponin I enzymes
• Myocardial contusion (trauma)
• Myocarditis
• Cardiomyopathy
• Post ischemic myocardial stunning
• Septic myocardial depression
• Pharmacologic
o Anthracycline cardiotoxicity
o Calcium channel blockers
Marc Imhotep Cray, M.D.
Cardiogenic (4)
20
• Mechanical
• -Valvular failure Regurgitant Obstructive
• -Hypertropic cardiomyopathy
• -Ventricular septal defect
• Arrhythmic
• -Bradycardia Sinus (e.g.,vagal syncope),
Atrioventricular blocks
• -Tachycardia SupraventricularVentricular
Marc Imhotep Cray, M.D.
Distributive shock
21
 Distributive shock results from excessive vasodilation
and impaired distribution of blood flow
• Septic shock is the most common form of
distributive shock and is characterized by
considerable mortality (treated, around 30%;
untreated, probably >80%)
• In United States, this is leading cause of
noncardiac death in intensive care units (ICUs)
Marc Imhotep Cray, M.D.
Distributive shock (2)
22
 Other causes of distributive shock include systemic
inflammatory response syndrome (SIRS) due to
noninfectious inflammatory conditions such as burns and
pancreatitis; toxic shock syndrome (TSS); anaphylaxis;
reactions to drugs or toxins, including insect bites,
transfusion reaction, and heavy metal poisoning;
addisonian crisis; hepatic insufficiency; and neurogenic
shock due to brain or spinal cord injury
Marc Imhotep Cray, M.D.
Distributive (3)
23
• Septic (bacterial, fungal, viral, rickettsial)
• Toxic shock syndrome
• Anaphylactic, anaphylactoid
• Neurogenic (spinal shock)
• Endocrinologic
• Adrenal crisis
• Toxic (e.g., nitroprusside, bretyllium)
24
Major pathogenic pathways in septic shock
Microbial products activate endothelial cells and cellular and humoral elements of the innate
immune system, initiating a cascade of events that lead to end-stage multiorgan failure.
DIC, Disseminated intravascular coagulation; HMGBI, high-mobility group box I protein; NO, nitric oxide; PAF, platelet-activating factor; PAI-I,
plasminogen activator inhibitor- I ; PAMP, pathogen- associated molecular pattern; STNFR, soluble tumor necrosis factor receptor; TF, tissue
factor; TFPI, tissue factor pathway inhibitor.
Robbins Basic Pathology 10e, Elsevier, 2018. Fig. 4.19, Pg. 117.
Marc Imhotep Cray, M.D.
Distributive shock (4) Capsule
25
Distributive shock
• As in hypovolemic shock, there is an insufficient
intravascular volume of blood
• This form of "relative" hypovolemia is result of
dilation of blood vessels which diminishes
systemic vascular resistance
• Examples of this form of shock are:
1. Septic shock
2. Anaphylactic shock
3. Neurogenic shock
Marc Imhotep Cray, M.D.
Obstructive shock
26
Obstructive shock
• In this situation flow of blood is obstructed which
impedes circulation and can result in circulatory
arrest
• Several conditions result in this form of shock, including:
1. Cardiac tamponade
2. Tension pneumothorax
3. pulmonary embolism
4. Aortic stenosis
Marc Imhotep Cray, M.D.
Extracardiac obstructive shock
Impaired diastolic filling (decreased preload)
27
High CVP, Low PCWP, Cardiac Output is usually decreased w increased SVR
• A physical impairment to adequate forward circulatory flow
involving mechanisms different than primary myocardial or
valvular dysfunction
• Frank decrease in filling pressures (as in mediastinal
compressions of great veins) or trends towards equalization of
pressures in case of cardiac tamponade or markedly increased
right ventricular filling pressures (Pulmonary arterial
hypertension [PAH])
Marc Imhotep Cray, M.D.
Endocrine shock
Recently a fifth form of shock has been introduced based
on endocrine disturbances.
28
Causes:
• Hypothyroidism, in critically ill patients, reduces cardiac output and
can lead to hypotension and respiratory insufficiency
• Thyrotoxicosis may induce a reversible cardiomyopathy
• Acute adrenal insufficiency is frequently the result of discontinuing
corticosteroid treatment without tapering the dosage
• However, surgery and intercurrent disease in patients on corticosteroid
therapy without adjusting dosage to accommodate for increased
requirements may also result in this condition
• Relative adrenal insufficiency in critically ill patients where present
hormone levels are insufficient to meet the higher demands
Marc Imhotep Cray, M.D.
Compensated vs.
decompensated shock
29
With compensated shock, body is experiencing a state of low blood
volume but is still able to maintain blood pressure and organ
perfusion by increasing heart rate and constricting blood vessels
Symptoms of compensated shock include:
 Agitation, restlessness and anxiety
 Altered mental status
 Tachycardia or tachypnea
 Change in pallor, cyanosis around the lips, or clammy skin
 Nausea or vomiting
 Thirst
 Weak, thready or absent pulse
 Narrowing pulse pressure
 Shallow, rapid breathing
 Mental status may be normal, in the early stages
Marc Imhotep Cray, M.D.
Compensated vs.
decompensated shock (2)
30
With compensated shock, body is able to take measures to maintain
blood pressure, however as shock worsens (decompensates), body
becomes unable to keep up perfusion of vital organs is no longer
maintained Lactic acidosis
Symptoms of decompensated shock include:
 Falling blood pressure (systolic of 90 mm Hg or lower with adults)
 Tachycardia and tachypnea
 Low urine output
 Labored and irregular breathing
 Weak, thready or absent peripheral pulses
 Ashy or cyanotic pallor
 Reduced body temperature
 Decreased mental status
 Dilated pupils
Marc Imhotep Cray, M.D.
Decompensated shock
31
 With decompensated shock, it may be necessary to request
advanced life support measures for patient
 Priority should be given to management of airway and
treatment of the underlying cause of shock
 A decrease in blood pressure is often an indication of late-
stage shock and treatment should start well before this is
detected
 If condition remains untreated will progress into irreversible
shock ultimately leads to death
Marc Imhotep Cray, M.D.
Comparison of types of shock
(Early stage)
32
Vasoconstrictive Vasodilatative
Hypovolamic Cardiogenic Circulatory Septic
Cardiac
index
Cardiac
index
Peripheral
resistance
Peripheral
resistance
Blood
Volume
Blood
Volume
NB: Malperfusion and organ dysfunction
are ultimate end point of any shock stage
Marc Imhotep Cray, M.D. 33
Decreased cardiac output
Decreased blood pressure
Decreased tissue perfusion
Decreased coronary perfusion
Decreased myocardial function
Microcirculatory
obstruction
Cellular aggregation
Microcirculatory damage
Cell hypoxia
Metabolic
acidosis
Decreased
myocardial
contraction
Inracellular
fluid
loss
Decreased
venous return
BP = CO x SVR
Pathophysiology Concept Map
Marc Imhotep Cray, M.D.
Treating Shock Capsule
34
 The key toward successfully treating shock is a rapid response
 If it can be treated before reaching decompensated phase, that is
best
 In many major life-threatening situations development of shock
should be anticipated
 EM providers refer to a ‘golden hour’ or ‘golden period’ in which
care should be delivered as quickly as possible and if it is, patient
will not suffer any lasting damage  requires a speedy assessment
of patient and rapid transport to a advance care facility
Marc Imhotep Cray, M.D.
Treatment of shock
35
Generalities: ABCs
Positioning, avoiding hypothermia
Maintaining adequate oxygenization
Fluid resuscitation
Pain relief ?
inotropic treatment?
Marc Imhotep Cray, M.D.
Enhance compensatory phase of
shock
36
• Maintenance of mean circulatory pressure
• Maximizing cardiac function
• Redistributing perfusion to vital organs
• Optimizing unloading of oxygen at tissues
Marc Imhotep Cray, M.D.
Maintain Blood Volume
37
• Fluid redistribution to
vascular space
• From interstitium
(Starling effect)
• From intracellular
space (osmotic effect)
• Decreased renal fluid losses
• Decreased glomerular
filtration rate (GFR)
• Increased aldosterone
• Increased vasopressin
Marc Imhotep Cray, M.D.
Mintain Blood Pressure
38
• Decreased venous capacitance
• Increased sympathetic activity
• Increased circulating (adrenal) epinephrine
• Increased angiotensin
• Increased vasopressin
Marc Imhotep Cray, M.D.
Maximize Cardiac Performance
39
• Increased contractility
• Sympathetic stimulation
• Adrenal stimulation
Marc Imhotep Cray, M.D.
Early mechanical ventilation
40
• allows blood flow to be redistributed
• tends to reverse lactic acidosis
• supports patient until other therapeutic measures
can be effective
Tidal volumes in order of 7-10 ml/kg of lean body mass, an
O2 concentration that results in arterial saturation not less
than 92%, adequate ventilator rate and sedation to minimize
the work of breathing.
Marc Imhotep Cray, M.D.
Fluid resuscitation
41
IV line c Large bore cannula
Choice of infusion
Sm. volume resuscitation (hypertonic NaCl solution)
General conditions: parameters ( BP, Pulse, CVP, SatO2 etc.)
Lactated Ringer's solution Colloids
Dextrane
Hydroethylstrach
Gelatine
Marc Imhotep Cray, M.D.
Inotropic drugs
42
Inotropie Heart rate SVR Kidney
Blood flow
Cornarry
Blood flow
Cardiac
Output
Dose
Epinephrin ++ + + - + +
10-30
mcg/min
Norepinephrin ++ 0 ++ -- + +
2-8
mcg/min
Dopamin ++ + - ++ + ++
2-5
mcg/min/kg
Dobutamin +++ (+) -- + + ++
5-15
mcg/min/kg
Isoproterenol ++ ++ - + + ++ 5 mcg/mi
Amrinon +++ 0 -- + + ++
Bolus 0.5 -
1.5 mg/kg
Cont.: 2 to
10
mcg/kg/min
Marc Imhotep Cray, M.D.
Summary of Shock
43
 Shock is defined as a state of systemic tissue hypoperfusion
resulting from reduced cardiac output and/or reduced effective
circulating blood volume.
 The major types of shock are cardiogenic (e.g., myocardial
infarction), hypovolemic (e.g., blood loss), and septic (e.g.,
infections).
 Shock of any form can lead to hypoxic tissue injury if not
corrected.
 Septic shock is caused by the host response to bacterial or fungal
infections; it is characterized by endothelial cell activation,
vasodilation, edema, disseminated intravascular coagulation, and
metabolic derangements.
Marc Imhotep Cray, M.D.
THE END
44
Marc Imhotep Cray, M.D.
Further Study:
45
Reading:
Robbins Basic Pathology 10e, Elsevier, 2018 ;Pgs. 115-118.
Sethi, AK et al. Shock-A Short Review. Indian J. Anaesth.
2003; 47 (5) : 345-359
Video Lectures:
Circulatory Shock_Dr. Najeeb

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Pathology and Pathophysiology of Shock

  • 1. Pathology and Pathophysiology of Shock Marc Imhotep Cray M.D.
  • 2. Marc Imhotep Cray, M.D. Learning Objectives 2 1. Discuss the general concepts associated with shock states, including physiologic response to shock, and shock progression. 2. Describe cardiogenic shock, including pathophysiology, clinical manifestations, diagnosis, and management. 3. Discuss hypovolemic shock, including pathophysiology, clinical manifestations, diagnosis, and management. 4. Explain the septic type of distributive shock, including pathophysiology, clinical manifestations, diagnosis, and management. By the end of this lecture the learner should be able to:
  • 3. Marc Imhotep Cray, M.D. Learning Objectives 3 5. Discuss the neurologic and anaphylactic types of distributive shock, including the pathophysiology, clinical manifestations, diagnosis, and management of each type. 6. Describe the major causes of obstructive shock, including the pathophysiology, clinical manifestations, diagnosis, and management of each cause 7. Discuss use of pharmacotherapy in the management of shock states. By the end of this lecture the learner should be able to:
  • 4. Marc Imhotep Cray, M.D. Shock Capsule 4  Shock is a clinical condition characterized by a fast pulse rate (usually > 100 beats/min) and a low blood pressure (systolic blood pressure usually < 100 mmHg)  Common types of shock are  hypovolemic (low blood volume, e.g. in hemorrhage),  cardiogenic (heart pump failure, e.g. in myocardial infarction)  septic (severe infection)  Less common types are  anaphylactic (type I hypersensitivity reaction, e.g. penicillin allergy)  neurogenic (loss of sympathetic vasomotor tone, e.g. in a spinal cord injury)
  • 5. Marc Imhotep Cray, M.D. Shock, Pathology of Different Types, Animation_Alila Medical Media 5Online Version
  • 6. Marc Imhotep Cray, M.D. Stages of Shock 6 As stated above Shock is a progressive disorder that leads to death if underlying causes are not corrected  Exact mechanisms of sepsis-related death are still unclear; aside from increased lymphocyte and enterocyte apoptosis, cellular necrosis is minimal • Death typically follows the failure of multiple organs usually offer no morphological clues to explain their dysfunction  For hypovolemic and cardiogenic shock pathways leading to a patient’s demise are reasonably well understood tissue ischemia, acute tubular necrosis, lactic acidosis severe cellular and tissue injury cardiopulmonary arrest  Unless insult is massive and rapidly lethal (e.g., exsanguination from a ruptured aortic aneurysm), shock tends to evolve through three general (albeit somewhat artificial) stages…
  • 7. Marc Imhotep Cray, M.D. The 3 Stages of Shock 7 These stages have been documented most clearly in hypovolemic shock but are common to other forms as well:  Stage 1 An initial nonprogressive stage during which reflex compensatory mechanisms are activated and vital organ perfusion is maintained  Stage 2 A progressive stage characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic derangement, including acidosis  Stage 3 An irreversible stage in which cellular and tissue injury is so severe that even if hemodynamic defects are corrected, survival is not possible
  • 8. Marc Imhotep Cray, M.D. Shock, Circulatory Defined 8 Circulatory shock, commonly known as just shock, is a serious, life- threatening medical condition where insufficient blood flow reaches body tissues  As blood carries oxygen and nutrients around body, reduced flow hinders delivery of these components to tissues, and can stop tissues from functioning properly The process of blood entering tissues is called perfusion, so when perfusion is not occurring properly this is called a hypoperfusional (hypo = below) state
  • 9. Marc Imhotep Cray, M.D. Shock (circulatory) 9 Effects of inadequate perfusion on cell function Learn more from Dr. Najeeb’s Video Series on Circulatory shock
  • 10. Marc Imhotep Cray, M.D. The problem in shock 10 From: http://www.cvpharmacology.com/clinical topics/hypotension.htm • Altered circulatory parameters • Compromised microcirculation • Persistent severe hypoxia • Multiple organ failure
  • 11. Marc Imhotep Cray, M.D. Main Types of Shock 11 Vasoconstrictive • Trauma, bleeding, burning, ileus (volumen loss) • Pulmonary embolism (impaired cardiac filling) • Myocardial infarction (impaired cardiac contraction) Vasodilatative • Anaphylaxis, sepsis (maldistribution of blood flow) • Spinal medullary injury (venous pooling) • Hypothermia
  • 12. Marc Imhotep Cray, M.D. Classification of Shock 12 • In 1972 Hinshaw and Cox suggested following classification which is still used today • It uses four types of shock: 1. hypovolemic 2. cardiogenic 3. distributive and 4. obstructive shock
  • 13. Marc Imhotep Cray, M.D. Classification (Based on cardiovascular characteristics, which was initially proposed in 1972 by Hinshaw and Cox.) 13 Hypovolemic Hemorrhagic Fluid depletion Increased vascular capacitance Cardiogenic Myopathic Mechanical Arrhythmic Distributive Septic, etc. Obstructive PE, pericarditis, pnumothorax etc.
  • 14. Marc Imhotep Cray, M.D. Hypovolemic shock 14 Hypovolemic shock This is most common type of shock and based on insufficient circulating volume = circulating shock • Its primary cause is loss of fluid from circulation from either an internal or external source • An internal source may be hemorrhage • External causes may include extensive bleeding, high output fistulae (greater than 500 ml per day)or severe burns
  • 15. Marc Imhotep Cray, M.D. Hypovolemic Shock 15 Low central venous pressure (CVP), Low pulmonary capillary wedge pressure (PCWP), Low cardiac output (CO) and cardiac index (CI), and high SVR arterial blood pressure may be normal or low Loss in circulatory volume • Decreased venous return • Decreased filling of cardiac chambers • Decreased cardiac output • increase in systemic vascular resistance (SVR)
  • 16. Marc Imhotep Cray, M.D. Hypovolemic Shock (2) Causes 16 Hemorrhagic • Trauma • Gastrointestinal • Retroperitoneal Fluid depletion (nonhemorrhagic) • External fluid loss • Dehydration • Vomiting • Diarrhea • Polyuria Interstitial fluid redistribution • Thermal injury • Trauma • Anaphylaxis Increased vascular capacitance (venodilation) • Sepsis • Anaphylaxis • Toxins/Drugs
  • 17. Marc Imhotep Cray, M.D. Cardiogenic shock 17 Cardiogenic shock This type of shock is caused by failure of heart to pump effectively • This can be due to damage to heart muscle, most often from a large myocardial infarction • Other causes of cardiogenic shock include o arrhythmias, o cardiomyopathy, o congestive heart failure (CHF), and o cardiac valve problems
  • 18. Marc Imhotep Cray, M.D. Cardiogenic Shock (2) 18 • dependent on poor pump function • acute catastrophic failure of LV pump function High PCWP, low CO and CI, and generally a high SVR
  • 19. Marc Imhotep Cray, M.D. Cardiogenic (3) 19 Myopathic • Myocardial infarction (left ventricle, right ventricle) • Elevations in CK-MB and Troponin I enzymes • Myocardial contusion (trauma) • Myocarditis • Cardiomyopathy • Post ischemic myocardial stunning • Septic myocardial depression • Pharmacologic o Anthracycline cardiotoxicity o Calcium channel blockers
  • 20. Marc Imhotep Cray, M.D. Cardiogenic (4) 20 • Mechanical • -Valvular failure Regurgitant Obstructive • -Hypertropic cardiomyopathy • -Ventricular septal defect • Arrhythmic • -Bradycardia Sinus (e.g.,vagal syncope), Atrioventricular blocks • -Tachycardia SupraventricularVentricular
  • 21. Marc Imhotep Cray, M.D. Distributive shock 21  Distributive shock results from excessive vasodilation and impaired distribution of blood flow • Septic shock is the most common form of distributive shock and is characterized by considerable mortality (treated, around 30%; untreated, probably >80%) • In United States, this is leading cause of noncardiac death in intensive care units (ICUs)
  • 22. Marc Imhotep Cray, M.D. Distributive shock (2) 22  Other causes of distributive shock include systemic inflammatory response syndrome (SIRS) due to noninfectious inflammatory conditions such as burns and pancreatitis; toxic shock syndrome (TSS); anaphylaxis; reactions to drugs or toxins, including insect bites, transfusion reaction, and heavy metal poisoning; addisonian crisis; hepatic insufficiency; and neurogenic shock due to brain or spinal cord injury
  • 23. Marc Imhotep Cray, M.D. Distributive (3) 23 • Septic (bacterial, fungal, viral, rickettsial) • Toxic shock syndrome • Anaphylactic, anaphylactoid • Neurogenic (spinal shock) • Endocrinologic • Adrenal crisis • Toxic (e.g., nitroprusside, bretyllium)
  • 24. 24 Major pathogenic pathways in septic shock Microbial products activate endothelial cells and cellular and humoral elements of the innate immune system, initiating a cascade of events that lead to end-stage multiorgan failure. DIC, Disseminated intravascular coagulation; HMGBI, high-mobility group box I protein; NO, nitric oxide; PAF, platelet-activating factor; PAI-I, plasminogen activator inhibitor- I ; PAMP, pathogen- associated molecular pattern; STNFR, soluble tumor necrosis factor receptor; TF, tissue factor; TFPI, tissue factor pathway inhibitor. Robbins Basic Pathology 10e, Elsevier, 2018. Fig. 4.19, Pg. 117.
  • 25. Marc Imhotep Cray, M.D. Distributive shock (4) Capsule 25 Distributive shock • As in hypovolemic shock, there is an insufficient intravascular volume of blood • This form of "relative" hypovolemia is result of dilation of blood vessels which diminishes systemic vascular resistance • Examples of this form of shock are: 1. Septic shock 2. Anaphylactic shock 3. Neurogenic shock
  • 26. Marc Imhotep Cray, M.D. Obstructive shock 26 Obstructive shock • In this situation flow of blood is obstructed which impedes circulation and can result in circulatory arrest • Several conditions result in this form of shock, including: 1. Cardiac tamponade 2. Tension pneumothorax 3. pulmonary embolism 4. Aortic stenosis
  • 27. Marc Imhotep Cray, M.D. Extracardiac obstructive shock Impaired diastolic filling (decreased preload) 27 High CVP, Low PCWP, Cardiac Output is usually decreased w increased SVR • A physical impairment to adequate forward circulatory flow involving mechanisms different than primary myocardial or valvular dysfunction • Frank decrease in filling pressures (as in mediastinal compressions of great veins) or trends towards equalization of pressures in case of cardiac tamponade or markedly increased right ventricular filling pressures (Pulmonary arterial hypertension [PAH])
  • 28. Marc Imhotep Cray, M.D. Endocrine shock Recently a fifth form of shock has been introduced based on endocrine disturbances. 28 Causes: • Hypothyroidism, in critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency • Thyrotoxicosis may induce a reversible cardiomyopathy • Acute adrenal insufficiency is frequently the result of discontinuing corticosteroid treatment without tapering the dosage • However, surgery and intercurrent disease in patients on corticosteroid therapy without adjusting dosage to accommodate for increased requirements may also result in this condition • Relative adrenal insufficiency in critically ill patients where present hormone levels are insufficient to meet the higher demands
  • 29. Marc Imhotep Cray, M.D. Compensated vs. decompensated shock 29 With compensated shock, body is experiencing a state of low blood volume but is still able to maintain blood pressure and organ perfusion by increasing heart rate and constricting blood vessels Symptoms of compensated shock include:  Agitation, restlessness and anxiety  Altered mental status  Tachycardia or tachypnea  Change in pallor, cyanosis around the lips, or clammy skin  Nausea or vomiting  Thirst  Weak, thready or absent pulse  Narrowing pulse pressure  Shallow, rapid breathing  Mental status may be normal, in the early stages
  • 30. Marc Imhotep Cray, M.D. Compensated vs. decompensated shock (2) 30 With compensated shock, body is able to take measures to maintain blood pressure, however as shock worsens (decompensates), body becomes unable to keep up perfusion of vital organs is no longer maintained Lactic acidosis Symptoms of decompensated shock include:  Falling blood pressure (systolic of 90 mm Hg or lower with adults)  Tachycardia and tachypnea  Low urine output  Labored and irregular breathing  Weak, thready or absent peripheral pulses  Ashy or cyanotic pallor  Reduced body temperature  Decreased mental status  Dilated pupils
  • 31. Marc Imhotep Cray, M.D. Decompensated shock 31  With decompensated shock, it may be necessary to request advanced life support measures for patient  Priority should be given to management of airway and treatment of the underlying cause of shock  A decrease in blood pressure is often an indication of late- stage shock and treatment should start well before this is detected  If condition remains untreated will progress into irreversible shock ultimately leads to death
  • 32. Marc Imhotep Cray, M.D. Comparison of types of shock (Early stage) 32 Vasoconstrictive Vasodilatative Hypovolamic Cardiogenic Circulatory Septic Cardiac index Cardiac index Peripheral resistance Peripheral resistance Blood Volume Blood Volume NB: Malperfusion and organ dysfunction are ultimate end point of any shock stage
  • 33. Marc Imhotep Cray, M.D. 33 Decreased cardiac output Decreased blood pressure Decreased tissue perfusion Decreased coronary perfusion Decreased myocardial function Microcirculatory obstruction Cellular aggregation Microcirculatory damage Cell hypoxia Metabolic acidosis Decreased myocardial contraction Inracellular fluid loss Decreased venous return BP = CO x SVR Pathophysiology Concept Map
  • 34. Marc Imhotep Cray, M.D. Treating Shock Capsule 34  The key toward successfully treating shock is a rapid response  If it can be treated before reaching decompensated phase, that is best  In many major life-threatening situations development of shock should be anticipated  EM providers refer to a ‘golden hour’ or ‘golden period’ in which care should be delivered as quickly as possible and if it is, patient will not suffer any lasting damage  requires a speedy assessment of patient and rapid transport to a advance care facility
  • 35. Marc Imhotep Cray, M.D. Treatment of shock 35 Generalities: ABCs Positioning, avoiding hypothermia Maintaining adequate oxygenization Fluid resuscitation Pain relief ? inotropic treatment?
  • 36. Marc Imhotep Cray, M.D. Enhance compensatory phase of shock 36 • Maintenance of mean circulatory pressure • Maximizing cardiac function • Redistributing perfusion to vital organs • Optimizing unloading of oxygen at tissues
  • 37. Marc Imhotep Cray, M.D. Maintain Blood Volume 37 • Fluid redistribution to vascular space • From interstitium (Starling effect) • From intracellular space (osmotic effect) • Decreased renal fluid losses • Decreased glomerular filtration rate (GFR) • Increased aldosterone • Increased vasopressin
  • 38. Marc Imhotep Cray, M.D. Mintain Blood Pressure 38 • Decreased venous capacitance • Increased sympathetic activity • Increased circulating (adrenal) epinephrine • Increased angiotensin • Increased vasopressin
  • 39. Marc Imhotep Cray, M.D. Maximize Cardiac Performance 39 • Increased contractility • Sympathetic stimulation • Adrenal stimulation
  • 40. Marc Imhotep Cray, M.D. Early mechanical ventilation 40 • allows blood flow to be redistributed • tends to reverse lactic acidosis • supports patient until other therapeutic measures can be effective Tidal volumes in order of 7-10 ml/kg of lean body mass, an O2 concentration that results in arterial saturation not less than 92%, adequate ventilator rate and sedation to minimize the work of breathing.
  • 41. Marc Imhotep Cray, M.D. Fluid resuscitation 41 IV line c Large bore cannula Choice of infusion Sm. volume resuscitation (hypertonic NaCl solution) General conditions: parameters ( BP, Pulse, CVP, SatO2 etc.) Lactated Ringer's solution Colloids Dextrane Hydroethylstrach Gelatine
  • 42. Marc Imhotep Cray, M.D. Inotropic drugs 42 Inotropie Heart rate SVR Kidney Blood flow Cornarry Blood flow Cardiac Output Dose Epinephrin ++ + + - + + 10-30 mcg/min Norepinephrin ++ 0 ++ -- + + 2-8 mcg/min Dopamin ++ + - ++ + ++ 2-5 mcg/min/kg Dobutamin +++ (+) -- + + ++ 5-15 mcg/min/kg Isoproterenol ++ ++ - + + ++ 5 mcg/mi Amrinon +++ 0 -- + + ++ Bolus 0.5 - 1.5 mg/kg Cont.: 2 to 10 mcg/kg/min
  • 43. Marc Imhotep Cray, M.D. Summary of Shock 43  Shock is defined as a state of systemic tissue hypoperfusion resulting from reduced cardiac output and/or reduced effective circulating blood volume.  The major types of shock are cardiogenic (e.g., myocardial infarction), hypovolemic (e.g., blood loss), and septic (e.g., infections).  Shock of any form can lead to hypoxic tissue injury if not corrected.  Septic shock is caused by the host response to bacterial or fungal infections; it is characterized by endothelial cell activation, vasodilation, edema, disseminated intravascular coagulation, and metabolic derangements.
  • 44. Marc Imhotep Cray, M.D. THE END 44
  • 45. Marc Imhotep Cray, M.D. Further Study: 45 Reading: Robbins Basic Pathology 10e, Elsevier, 2018 ;Pgs. 115-118. Sethi, AK et al. Shock-A Short Review. Indian J. Anaesth. 2003; 47 (5) : 345-359 Video Lectures: Circulatory Shock_Dr. Najeeb