Understanding the Pathophysiology and Management of Shock

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:

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:

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)

Shock, Pathology of Different Types,
Animation_Alila Medical Media
5Online Version

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…

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

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

Shock (circulatory)
9
Effects of inadequate perfusion on cell function
Learn more from Dr. Najeeb’s Video Series on Circulatory shock

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

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

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

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.

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

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)

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

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

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

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

Cardiogenic (4)
20
• Mechanical
• -Valvular failure Regurgitant Obstructive
• -Hypertropic cardiomyopathy
• -Ventricular septal defect
• Arrhythmic
• -Bradycardia Sinus (e.g.,vagal syncope),
Atrioventricular blocks
• -Tachycardia SupraventricularVentricular

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)

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

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.

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

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

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])

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

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

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

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

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

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

Treatment of shock
35
Generalities: ABCs
Positioning, avoiding hypothermia
Maintaining adequate oxygenization
Fluid resuscitation
Pain relief ?
inotropic treatment?

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

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

Mintain Blood Pressure
38
• Decreased venous capacitance
• Increased sympathetic activity
• Increased circulating (adrenal) epinephrine
• Increased angiotensin
• Increased vasopressin

Maximize Cardiac Performance
39
• Increased contractility
• Sympathetic stimulation
• Adrenal stimulation

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.

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

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

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.

THE END
44

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

Understanding the Pathophysiology and Management of Shock

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