The complication of shock with classification

Shock
Red:very important.
Green: Doctor’s notes.
Pink: formulas.
Yellow: numbers.
Gray:notes and explanation.
Physiology Team 436 – Cardiovascular Block Lecture 11
Lecture: If work is intended for initial studying.
Review: If work is intended for revision.
1

Objectives
2
⦁ T
ypes and causes of shock.
⦁ Define circulatory shock.
⦁ Mechanisms responsible for the irreversible phase of hemorrhagic shock.
⦁ Body compensatory mechanisms during reversible phases of hemorrhagic shock.
⦁ Define shock and state the pathophysiological classification of shock.
⦁ Describe the pathways leading to shock and decreased tissue perfusion.
⦁ Discuss the stages of a hypovolemic shock.
⦁ Explain how stage III hypovolemic shock might result in major organs failure.
⦁ Discuss the different compensatory mechanisms during a hypovolemic shock.
⦁ Describe the positive feedback mechanisms in the irreversible stage of a hypovolemic shock.
Study Smart:focus on mutual topics.

The cell is the basic unit of life and it needs oxygen to produce
energy.
No oxygen  No energy  No life
Circulatory shock: When the circulatory system is unable to
provide adequate circulation & tissue perfusion  decreased
availability of oxygen and nutrients  failure to deliver oxygen
to the tissues & vital body organs relative to its metabolic
requirement  cellular hypoxia and energy deficit .
Result: organ dysfunction and cellular damage.(not death)
If not quickly corrected: whole body failure  leads to
irreversible shock and death.
Shock
ONLY IN MALES’ SLIDES
Shock may be defined as a
pathophysiological state in
which there is :
1 widespread
2serious reduction of tissue
perfusion
which if prolonged :leads to
generalized impairment of
cellular function.
Video of (Shock)
Duration: (9;10 mins)
Video of (Shock)
Duration: (16:28 mins)
3

Pathways Leading to Decreased Tissue Perfusion and Shock
Decreased tissue perfusion
 Causes: hemorrhage / hypovolemia - cardiac failure -
neurologic injury
.
 Result: immune and inflammatory responses.
 Alternatively, elaboration of microbial products during infection
or release of endogenous cellular products from tissue injury
→ cellular activation → influences tissue perfusion and the
development of shock .
Systemic hypotension
o N ORMAL BP :120/
80
o L OW BP < 90/60
o Arterial pressure = cardiac output x systemic vascular resistance
o Reduction in either component (cardiac output or vascular
resistance) without a compensatory elevation of the other
will result in hypotension.
4

Types of Shock
Circulatory Shock
Low output shock
Hypovolemic Cardiogenic
-Is associated with loss of40% or more of
left ventricle myocardial function.
- Mortality rate:60%-90%
Obstructive
High/Normal output
shock
Distributive
Vasogenic:Septic/toxic,Anaphylactic,
Psychogenic
Spinal:neurogenic
MAP = CO X PR
(the problem is low cardiac output)
MAP = CO X PR
(the problem is in peripheral resistance)
Full playlist of Khan Academy’s Shock-related videos
5

Causes and Classification of Shock
6
TYPE CAUSES SYMPTOMS AND SIGNS
• Bleeding/ Hemorrhage (internal/external) (Most Common)
1. Hypotension (≤ 85/40mmHg) ;weak but rapid pulse .
2. Tachycardia (Compensation for↓ MAP sensed by
Baroreceptors) Rapid, weak, & thready pulse
(140/min).
Hypovolemi
c shock
(most
common)
• dehydration (sever vomiting,sever diarrhea, excess sweating)
• plasma loss (as in burns ,trauma)  low blood volume
3. Cool, clammy skin
4. Tachypnea “rapid respiration” (Compensation for
hypoxia sensed by Chemoreceptors) shallow
breathing , anxiety
Lead to: Reduced venous return (preload) loss of 15-25% of CO /1-2 L
hypotension
5. Restlessness due to hypo-perfusion.
6. Altered mental state
7. Oliguria (low urine output)/
8. Anuria (no urine output).
9. Blood test: Lactic acidosis.
Cardiogeni
c shock
Heart problems (e.g.,myocardial infarction(Most common), heart failure ,cardiac dysrhythmias) 
despite adequate ventricular fillingpressure ↓ contractility ↓in stroke volume ↓cardiac output
 hypotension
Myocarditis, cardiomyopathy, cardiac tamponade, congestive
heart failure Acute valvular dysfunction (e.g.,rapture of papillary
muscles post MI)
Sustained arrhythmias (e.g. heart block, ventricular
tachycardia) pulmonary embolism
Is associated with loss of > 40% of LV myocardial function, mortality rate is high 60-90%
1. Just like symptoms of a hypovolemic shock +
2. Distended jugular veins
3. Cardiomegaly
4. Congestion of lungs & viscera: Chest X-ray (CXR):
5. Interstitial pulmonary /Alveolar edema .
6. May be absent pulse
Obstructiv
e shock
• Obstruction of venous return:likeVena Cava syndrome (usually neoplasms)
• Compression of heart:like hemorrhagic pericarditis > cardiac tamponade
• Obstruction of outflow:like aortic dissection*, massive pulmonary embolism, pneumothorax.
• Circulatory obstruction (e.g.,constrictive pericarditis )
Lead to :reduced blood flow to lungs ↓ cardiac output  hypotension
1. Just like symptoms of a hypovolemic shock
+
2. Distended jugular veins
3. Pulses paradoxes (in cardiac tamponade).
* Aortic dissection:aorta is weak,a cyst becomes a parallel vessel to aorta and makes it rupture > sudden death.

Causes and Classification of Shock
Septic shock: infection  release of bacterial toxins  activation of NOS in
macrophages  production of NO  vasodilation + endothelial injury 
decreased vascular resistance hypotension
Anaphylactic shock: allergy (release of histamine)  IgE Mediated hypersensitivity
(histamine triggers peripheral vasodilation and an increase in capillary permeability
 decreased vascular resistance hypotension
Neurogenic shock:/Spinal Shock (venouspooling):spinal injury ↓ peripheral
vasomotor tone  loss of autonomic and motor reflexes  vasodilation 
Blood volume remains normal ↓in peripheral vascular resistance ↓ cardiac
output as bloodis pooled in peripheral veins  ↑ Capacityofblood↓
Venousreturn hypotension (Behaves likehypovolemicshock)
Psychogenicshock : stress, pain, or fright  ↓ HR & vesselsdilate
 Brain becomeshypo perfused  Loss ofconsciousness.
 Septic shock: Patient flushed & warm
due to his hyperdynamic state -
Severe drop in BP or hemoglobin-
fever – warm- sweaty skin and
hypotension
1-Vasogenic
 Anaphylatic shock: hypotension- skin
eruptions- breathlessness-
coughing - localized edema- weak -
rapid pulse
2- Low-
resistanc
e shock
 Neurogenic shock: as for
hypovolemic except warm, dry
skin
 Psychogenicshock : Simple
fainting (syncope)
High/Normal Cardiac Output Shock (Distributive)
MAP = CO X PR
(the problem is in vascular/peripheral resistance)
7

Pathophysiology of Shock
Reduce capillary
perfusion
Inadequate tissue
oxygen
Shift to anaerobic
metabolism
Metabolic
acidosis
Release of free radical and oxidative stress
- Reactive Oxygen Species
(ROS)
Tissue damage
Apoptosis
(programed cell
death)
8

Metabolic Changes & Cellular Response to Shock
1- Reduced capillary perfusion:
2-After 3-5 hours of shock:
3- granulocytes accumulation at injured vessels:( Free radical release and further tissue damage).
4- damage in GIT mucosa :allows bacteria into circulation.
Spasm of pre-post
capillary sphincters
Hypoxic tissue
damage
(oxidative stress)
Anaerobic
metabolism
( anaerobic
glycolysis)
Lactic acid
production
Metabolic acidosis
(intracellular
acidosis)
Failure of Na/k
pump
( Na & Ca inside
the cell)
Lysosomes, nuclear
membranes &
mitochondrial
breakdown
ONLY IN FEMALES’ SLIDES
Precapillary sphincters
dilate
Venules are still
constricted.
Blood stagnation in
capillaries.
Hypoxia continue +Fluid
leaves extra vascular
compartment.
(which will drain in
lymphatic vessel)
Further reduction in
circulating blood volume.
‫ﯾحور‬ ‫ﻻﻧﮫ‬ ‫ﻟﻔوﻟﯾمو‬ ‫ا‬
‫ل‬ ‫ﺑﯾﻘ‬
‫ﻟﻠﻣﻔﺎﺗﯾك‬
9

5- cerebral ischemia
6- Myocardial ischemia
acidosis).
depressed contractility+ myocardial damage(more shock and
7respiratory distress syndrome occurs :due to damage of capillary endothelial cells & alveolar
epithelial cells with release of cytokines.
8 multiple organ failure and death.
Cont.
depression of vasomotor center
(sympathetic)
vasodilation+ HR
further decrease in blood
pressure
10

Regulation
of BP
Short term
mechanisms
Baroreceptor
reflex
Chemoreceptor
reflex
CNS ischemic
response
Atrial reflexes
Intermediate and
long term
mechanisms
Hormonal
Catecholamines ADH
Renal
Other
Capillary shift
Increased 2,3
DPG
Restoration of
plasma volume
Restoration of
plasma proteins
Restoration of
RBCs
Short-term compensatory reactions:
are rapid and act within seconds to minutes
Intermediate-long term compensatory reactions:
are activated within hours or From hours to days
Compensatory Mechanisms During Hypovolemic Shock
Other compensatory reactions:
are activated within hours From hours to days
1. Cardiovascular.
2. Respiratory.
3. Endocrine.
4. Renal.
5. Others.
Video of (Compensatory Mechanisms of (Medical) Shock)
Duration: (18:48 mins)
11

Compensatory Mechanisms (The Important Ones)
Baroreceptor reflex by decreased blood pressure
Sympathetic stimulation
Chemoreceptors reflex by acidosis
Angiotensin II +III: powerful vasoconstrictors
Renin-Angiotensin mechanism
stimulation
Aldosterone:Na & water retention
Compensatory
mechanism
Release of antidiuretic
hormone (vasopressin)
Water retention
Vasoconstriction and thirst
stimulation
Plasma protein synthesis
Fluid shift mechanism
12

Short-Term Compensatory Mechanisms;
1- Arterial Baroreceptor Reflex
Flow to the heart and brain is maintained;reductions in flow to other organs.
14 Fully explained in arterial pressure regulation lecture.

Cont.
Total
physical
resistanc
e
Mean Arterial pressure

⦁ Reductions in mean arterial blood pressure (MAP) below 60:
1. do not evoke any additional responses through the baroreceptor reflex.
2. stimulates peripheral chemoreceptors (aortic bodies,carotid bodies,heart) that sense changes in pO2, pCO2, and
pH through tissue hypoxia and lactacidosis.
⦁ This results in:
 Enhancement of the existing tachycardia and vasoconstriction
 Respiratory stimulation → tachypnea
Short Term Compensatory Mechanisms;
2- Arterial Chemoreceptor Reflex

Vasoconstriction
(arteriolar constriction):this increasesTPR and hence MAP.
It is produced by:
o Baroreceptor reflex.
o Chemoreceptor reflex.
o Noreadrenaline-adrenaline vasoconstrictor mechanism (due to
activation ofadrenal medulla).
o Vasoconstriction is also produced by vasopressin-vasoconstrictor
mechanism (in subsequent slides).
Marked in:
o Skin:cold,pale.
o kidneys:drop in GFR & urine volume.
o Viscera.
o Flow to the heart and brain is maintained;reductions in flow to
other organs.
Important in:
o Shifting blood from the venous reservoir into the circulation.
o Maintaining filling pressure of the heart.
Tachycardia
Produced by:
• Baroreceptor reflex.
• Chemoreceptor reflex.
• Increased sympathetic activity
.
Tachypnea
Caused by :activation of chemoreceptor reflex and
sympathetic over activity
.
Importance:
• Increase O2 delivery
.
• Increase thoracic pump activity→ help
venous return.
• The increased sympathetic activity also
causes restlessness → ↑ skeletal muscle activity
→ help venous return.
Compensatory Mechanisms During Hypovolemic Shock
Arterial Baroreceptor and Chemoreceptor Reflexes
17

Compensatory Mechanisms During Hypovolemic Shock;
Endocrine and Renal
18
Mechanism:
1. Release of hormones that initiate vasoconstriction.
2. Renal conservation of salt and water
.
3. Stimulation of hematopoeisis by erythropoietin
These compensatory reactions are activated:
Within hours
From hours to days
Endocrine and Renal Compensatory Mechanisms
o ↑ Circulating
vasoconstrictors
o Stimulation of sympathetic nervous system  release of epinephrine,norepinephrine from the adrenal medulla
(sympatho-adrenal axis) .
o Epinephrin is released almost exclusively from adrenal medulla where as norepinephrin is released from adrenal
medulla and sympathetic nerve endings.
o Vasoconstriction.
o ADH is actively secreted by the posterior pituitary gland in response to hemorrhage.
o Thus,hemorrhage  stimulates posterior pituitary  synthesis and release of vasopressin (ADH).
o ADH is potent vasoconstrictor.
o It also stimulates reabsorption of water.
o ↓ renal perfusion  secretion of renin from juxtaglomerular apparatus  generates angiotensin II 
o Angiotensin II is a powerful vasoconstrictor

o ↑ secretion of
glucocorticoids
by
adrenal cortex
o This helps to maintain blood glucose
o Stimulation
of
hematopoies
is
o ↓ blood volume & hypoxia  synthesis of erythropoeitin (EPO)  hematopoiesis.
o Renal conservation
of salt and
water
o Vasopressin  ↑ water reabsorption  ↑ blood volume  ↑ arterial pressure.
o Angiotensin II  release of aldosterone  ↑ salt reabsorption  ↑ blood
volume  ↑ arterial pressure.
o ↓ arterial pressure in kidney  ↓ decreases glomerular filtration rates and
thereby decreases the excretion of water and electrolytes directly
19
Cont.

These compensatory reactions are activated within hours or from hours to days
1.Responses activated: within hours
 Increased movement of interstitial fluid into capillaries (capillary fluid shift).
 Increased 2,3 DPG concentration in RBCs:This is important to help Hb deliver more O2 to the tissues (shift
O2 dissociation curve to the right).
2.Responses activated: within hours-days
 Restoration of circulatory plasma volume:takes 12-72 hrs after moderate hemorrhage.
 Restoration of plasma proteins:this occurs in 2 stages:
 Rapid entry of preformed albumin from extracellular stores.
 Hepatic synthesis of proteins over 3-4 days.
 Restoration of RBCs: this occurs in 2 stages:
 Increase RBCs count in response to erythropoietin within 10 days.
 Restoration of red cell mass within 4-8 weeks.
Other Compensatory Mechanisms During Hypovolemic Shock
20

In Normal Microcirculation
InterstitialFluid NFP = +5 to +10 mmHg
NFP = - 5 to -7mmHg
Hydrostatic Pressure = 0 mmHg
Venous Blood
Hydrostatic Pressure
18-20 mmHg
Blood Capillary
Colloid Osmotic Pressure
25 mmHg
ArterialBlood
30-35 mmHg
mmHg
 At arterial end: Water moves out of the capillary with a NFP of +5 to +10
Hydrostatic pressure dominates at the arterial end & net fluid flows out of the circulation.
 (Arterial pressure - Colloid osmotic pressure = + NFP filtration to interstitial fluid)
 At venous end: Water moves into the capillary with a NFP of -5 to -7 mmHg. Oncotic pressure
dominates at the venous end & net fluid will flow into the bloodstream.
 (Venous pressure - Colloid osmotic pressure = - NFP filtration to blood stream)
21 NFP = Net Filtration Pressure
Interstitial fluid

Fluid-Shift Mechanism
⦁ In shock,the hydrostatic pressure decreases & oncotic pressure is constant,as a result:
• The fluid exchange from the capillary to the extracellular space decreases.
• The fluid return from the extracellular space to the capillary increases.
⦁ That will increase the blood volume & will increase BP helping to compensate shock.
⦁ The capillary fluid shift mechanism means simply that anytime capillary pressure falls too low, fluid is absorbed
from the tissues through the capillary membranes and into the circulation, thus building up blood volume and
increasing the pressure in the circulation.
Normally During Fluid-Shift
22

Fluid-Shift Mechanism in Shock
10mmHg
Hydrostatic pressure
20mmHg
Hydrostatic Pressure 0mmHg
Decrease outflow
Increase inflow
23
Interstitial fluid
Venous Blood
Blood Capillary
Colloid Osmotic Pressure
25mmHg
Arterial Blood

24
Stages of Shock
Stage 1  pressure and cardiac output
are maintained (in recumbent position)
are not maintained ( 10-20 mmHg
drop)
decrease is life threatening
During Hypovolemic Shock :
Pressure decreases ,HR increases
Bicarbonate decrease, Lactic
increases
acid

Stages of Shock
Reversible shock:
(Compensated)
• Changes can be
reversed by
compensatory
mechanism
• (neurohormonal
activation) or by
treatment.
• Defense
mechanisms are
successful in
maintaining
perfusion.
• Non-progressive
Progressive
• Defense
mechanisms begin
to fall.
• Multi-organ
failure.
Irreversible shock:
• Complete failure
of compensatory
mechanisms.
• Can lead to death.
Shock
Stimulus
25
LysosomalActivation,
Release Proteases
Splitting of Plasma
Proteins
Vasoactive Peptides,
Amines,etc.
Hypotension,
Fluid Loss
Irreversible
Shock
Possible Mechanism in the
Development of Irreversible Shock

Stage 2 (Progressive Stage)
Happen if:When 20-40% of blood volume are lost,cardiac output cannot be
maintained and falls markedly
,even in the recumbent position.
Result in:
1Fluid also moves from the interstitial to the intravascular compartment
(i.e.,reabsorption of tissue fluids).
2 there will be massive activation of the sympathetic nervous system 
Leading to:
 intense arteriolar constriction in the vascular beds of the kidney
, gut,
and skin  redistribution of blood flow (i.e., centralization of blood
flow) with larger fractions going to the vital organs (heart and brain)
and smaller fractions going to the kidney
, gut, and skin. Despite intense
arteriolar constriction,systolic arterial BP declines by 10 to 20 mm Hg.
 generalized vasoconstriction (increasing blood volume in the central
circulation and tending to sustain venous return)
Stage 1 (Compensatory Stage)
Happen in: In healthy individuals, acute blood loss of 10 –
15 % of the normal blood volume (e.g.,blood donation)
Results in :activation of the sympathetic nervous system.
Symptoms:
• Arterial pressure is maintained
• Pressure decline when the patient assumes the erect
position
• Increase in heart rate,Paleness andAnxiety
Compensation is achieved acutely by:
• Increase in heart rate.
• Constriction of the arterioles.
 Thus, cardiac output is normal or slightly reduced
especially when the patient assumes the erect
position
Stages of Shock
26

Cont.
Stage 3
The compensatory mechanisms are maximally mobilized
in stage II.Thus,
Happen during : small additional losses of blood (>40 %)
can result in life-threatening reduction in cardiac output,
BP and tissue perfusion.
 Blood flow to heart, brain and kidney is further
reduced  severe ischemia and irreversible tissue
damage  this may result in impaired organ function
and death.
 The severe vasoconstriction may itself become a
complicating factor and initiate a vicious cycle
The factors that determine the ultimate outcome include:
• Duration of stage III.
• Severity of tissue anoxia.
• Age and condition of the patient.
27
Stage 2
(maximal mobilization of compensatory mechanisms)
Symptoms,signs and complications:
 Systolic arterial blood pressure declines by 10-20 mmHg
 T
achycardia (heart rate increases and pulse is thready and
weak)
 Skin is pale and cool (peripheral pallor is common)
 Deterioration of the mental state because the brain is getting
less oxygen. Patient looks weak, tired and drowsy. Patient may
show anxiety
,aggressiveness,and restlessness.
 Thirst.
 Oliguria (urine output is decreased).
 Angina may occur in patients who have intrinsic coronary
vascular disease.
 pH drops and metabolic acidosis develops due to increased
anaerobic glycolysis

Irreversible Stage of Hypovolemic Shock (Stage 3)
Mechanism In the irreversible stage of hypovolemic shock,a series of positive feed back mechanisms take place,leading to 
1- further deterioration in cardiac output and MAP
2- more tissue hypoxia
Depending on:the amount of blood lost
How :When blood loss is excessive and not immediately replaced,and proper treatment is delayed,this stage is reached and the patient dies.
In this stage,there is also failure of compensatory mechanisms.
The severe vasoconstriction may itself become a complicating factor and initiate a vicious cycle.It could happen also during irreversible stage
of hypovolemic shock
Mechanism:
1 Impaired coronary perfusion  cardiac ischemia  depression of cardiac function  further lowering of cardiac output.
2Reduced blood flow to the vasomoter centers in the medulla depresses the activity of compensatory reflexes  vasomotor failure  depression of
the activity of compensatory reflex  depression of cardiac function  further lowering of cardiac output.
3 Prolonged renal ischemia  acute tubular necrosis  may lead to prolonged post-shock renal insufficiency
.
4Bowel ischemia  breakdown of the mucosal barrier .This may lead to entry of bacteria and toxins into the circulation  depression of cardiac
function  further lowering of cardiac output
Generalized cellular deterioration:
• ↓ Mitochondrial activity inside the cells →↓ inATP
.
• ↓ of cellular metabolism,especially glucose →↓ inATP
.
• ↓ in active transport of Na+ and K+ across the cell → Na+ accumulation inside the cell.
• Rupture of many lysosomes.
28

Link to Editing File
(Please be sure to check this file frequently for any edits or updates on all of our lectures.)
References:
• Girls’and boys’slides.
• Guyton and HallTextbook of Medical Physiology (Thirteenth Edition.)
Quiz
29
🞂 https://www.onlineexambuilder.com/shock/exam-142187

Thank you!
30
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