Complete detail of shock

2. Shock

3.  Shock is a condition in which diminished cardiac
output or reduced effective circulating blood volume
impairs tissue perfusion and leads to cellular hypoxia.
 At the outset, the cellular injury is reversible; however,
prolonged shock eventually leads to irreversible tissue
injury and is often fatal.

4.  Heart Conditions:
They can be Heart attack, Heart failure etc.
 Heavy Bleeding:
It can be external or internal such as serious injury or
rupture of blood vessels.
 Dehydration:
Loss of fluid or plasma from the body.
 Severe allergic reactions:
May be caused due to any allergen like spores, dust
such as Anaphylactic shock.

5.  Spinal injuries:
Any damage to spinal cord or spinal nerve may
initiate the shock such as neurogenic shock.
 Severe burns:
They include internal and external burns like skin
burns
 Persistent vomiting or diarrhea:
Because it causes heavy loss of fluid or water.
 Poisoning:
It can damage the vital organs leading to shock and
death.

6.  Trauma:
It damages the brain as a result of distressing event.
 Pancreatitis:(inflammation of pancreas)
 Microbial infections:
Sepsis occurs because of any bacteria, fungi, or viral
infections leads to shock(septic).
 Excessive use of diuretics:
Due to excessive urination dehydration occurs
leading to the shock.

7.  Actually shock is divided into three types on the
basis of its causes
 Cardiogenic Shock:
(Due to cardiac abnormalities)
 Hypovolemic Shock:
(Due to plasma or fluid loss)
 Septic Shock:
(Due to infections)

8.  Cardiogenic shock (CS) is a medical emergency
resulting from inadequate blood flow due to the
dysfunction of the ventricles of the heart
 During this condition your heart cannot pump enough
blood and oxygen to the brain, kidneys, and other vital
organs of your body.

9.  The main cause of the cardiogenic shock in most
cases is the Heart Failure.
 Other possible causes of cardiogenic shock include:
 Inflammation of the heart muscle (myocarditis)
 Infection of the heart valves (endocarditis)
 Weakened heart from any cause
 Drug overdoses or poisoning
 Cardiac Arrhythmias

10.  In most cases, a lack of oxygen to your heart, usually
from a heart attack, damages its main pumping
chamber (left ventricle).
 Without oxygen-rich blood circulating to that area of
your heart, the heart muscle can weaken and go into
cardiogenic shock.
 Other factors also involved as given in the diagram.

12.  Anxiety, Restlessness
 Low blood pressure
 Shortness of breath
 Oliguria (low urine production)
 Pulmonary edema
 Weak Pulse
 Abnormal heart rhythms
 Fatigue etc.

13.  Hypovolemic shock is a medical emergency that
results from low cardiac output due to loss of blood
or plasma volume.
 The hypovolemic shock could be due to severe
dehydration through a variety of mechanisms or
from blood loss.
 People with hypovolemic shock have severe
hypovolemia with decreased peripheral perfusion.
 If left untreated, these patients can develop ischemic
injury of vital organs, leading to multi-system organ
failure.

14.  There are two main causes of hypovolemic shock:
1. Blood loss (haemorrhage):
Blood loss mostly occurs due to
 Trauma e.g. Gastrointestinal bleeding.
Other causes of hemorrhagic shock include:
 Bleed from an ectopic pregnancy
 Bleeding from surgical intervention

15.  Fluid loss:
Hypovolemic shock as a result of extracellular fluid
loss can be of the 4 etiologies. Fluid can be lost
through:
1. GI tract
2. Kidneys
3. Skin
4. Third spacing

16.  Hypovolemic shock results from depletion
of intravascular volume, whether by extracellular
fluid loss or blood loss.
 The body compensates with increased sympathetic
tone resulting in increased heart rate,
increased cardiac contractility, and peripheral
vasoconstriction.
 The first changes in vital signs seen in hypovolemic
shock include an increase in diastolic blood
pressure with narrowed pulse pressure.

17.  As volume status continues to decrease, systolic blood
pressure drops.
 As a result, oxygen delivery to vital organs is unable to
meet the oxygen needs of the cells.
 Cells switch from aerobic metabolism to anaerobic
metabolism, resulting in lactic acidosis.
 As sympathetic drive increases, blood flow is diverted
from other organs to preserve blood flow to the heart
and brain.
 This propagates tissue ischemia and worsens lactic
acidosis. If not corrected, there will be worsening
hemodynamic compromise and, eventually, death.

18.  Rapid heartbeat
 Quick, shallow breathing
 Feeling weak
 Being tired
 Confusion or wooziness
 Having little or no pee
 Low blood pressure
 Cool, clammy skin

19.  Septic shock is a potentially fatal medical condition
that triggered by microbial infections and is
associated with severe systemic inflammatory
response syndrome (SIRS).
 Systemic inflammatory response syndrome (SIRS), is
an inflammatory state affecting the whole body. It is
the body's response to an infectious or noninfectious
insult.
 Septic shock is responsible for 2% of all hospital
admissions in the United States.

20.  A bacterial, fungal, or viral infection can cause
sepsis.
 Most cases of septic shock are caused by gram-
positive bacteria, followed by endotoxin-
producing gram-negative bacteria, although fungal
infections are an increasingly prevalent cause of
septic shock.

21.  Sepsis commonly originates from:
1. Abdominal or digestive system infections
2. Lung infections like pneumonia, urinary tract
infection
3. Reproductive system infection
 In addition to microbes, SIRS may be triggered by a
variety of insults including burns, trauma or
pancreatitis.

22.  The common pathogenic mechanism is a massive
outpouring of inflammatory mediators from innate
and adaptive immune cells that produce arterial
vasodilation, vascular leakage, and venous blood
pooling. These cardiovascular abnormalities result in
tissue hypoperfusion, cellular hypoxia, and
metabolic derangements that lead to organ
dysfunction and, if severe and persistent, organ
failure and death.

24. Early Symptoms:
 Fever usually higher than 101˚F (38˚C)
 Low body temperature (hypothermia)
 Fast heart rate
 Rapid breathing, or more than 20 bpm
Severe Sepsis Symptoms:
 Noticeably lower amounts of urine
 Acute confusion
 Dizziness
 Bluish discoloration of the digits or lips (cyanosis)

25.  Shock is a progressive disorder that leads to death if
the underlying problems are not corrected.
 Death typically follows the failure of multiple organs,
which usually offer no morphological clues to explain
their dysfunction.
 Unless the insult is massive and rapidly lethal, shock
tends to evolve through three general stages:
1. Initial Non progressive Stage
2. Progressive Stage
3. Irreversible Stage

26.  It is the stage during which reflex compensatory
mechanisms are activated and vital organ perfusion
is maintained.
 In the early non progressive phase of shock, various
neurohumoral mechanisms help maintain cardiac
output and blood pressure.
 These mechanisms include baroreceptor reflexes,
release of catecholamines and anti-diuretic
hormone, activation of the renin-angiotensin-
aldersterone axis, and generalized sympathetic
stimulation.

27.  The net effect is tachycardia, peripheral
vasoconstriction, and renal fluid conservation.
 Cutaneous vasoconstriction causes the characteristic
“shocky” skin coolness and pallor.
 Coronary and cerebral vessels are less sensitive to
sympathetic signals and maintain relatively normal
caliber, blood flow, and oxygen delivery.
 Thus, blood is shunted away from the skin to the
vital organs such as the heart and the brain.

28.  If the underlying causes are not corrected, shock
passes imperceptibly to the progressive phase,
which as noted is characterized by widespread tissue
hypoxia, tissue hypoperfusion and onset of
worsening circulatory and metabolic derangement,
including acidosis.
 With widespread tissue hypoxia, vital organs are
affected and begin to fail.

29.  In the absence of appropriate intervention, or in
severe cases, the process eventually enters an
irreversible stage.
 It is the stage in which cellular and tissue injury is so
severe that even if the hemodynamic defects are
corrected, survival is not possible.
 Despite the best therapeutic interventions, the
downward spiral frequently culminates in death.

30.  Regardless of the cause, when tissues of the body
are not supplied with oxygen, body tries to remedy
the situation by initiating the series of neural and
harmonally mediated compensatory mechanisms.
 The end goal of these mechanisms to increase the
cardiac output and blood vessel tone to better
supply the cells with the oxygen.
 These compensatory mechanisms are grouped into
three categories:

31.  Acute compensatory mechanism:
Rapid action in minutes.
 Moderate compensatory mechanism:
Take action in 10 mins to 1 hour.
 Chronic compensatory mechanism:
It occurs in 1 hour to 48 hours.

32.  Acute compensatory mechanisms are limited to
those affecting the heart rate and redistributing the
peripheral blood back to the heart.
 Catecholamines:
They are mediated by sympathetic nervous system.
And catecholamines release and take effect within
30 secs to few minutes.

33.  Cortisol:
Cortisol is also rapidly mobilized in acute stages of
shock. Cortisol is released from adrenal gland having
many effects but stimulation of glycolysis and
mobilization of fat and protein stores for the
gluconeogenesis are most important.
Actually it provides energy in the form of glucose to
the body.

34.  Transcapillary Shifts:
A final mechanism that aids in acute improvement in
blood volume is transcapillary shifting of fluid.
It happens at capillary level, primiraly in cases of
hypovolemic shock.
When pressure in capillaries drop secondry to
hypovolemia, starling forces dictate that fluid will
move from an area of higher pressure to that of
lower pressure.

35.  The next level of compensation starts withiin about
10 mins after body has entered into the shock state.
 Angiotensin II:
Baroreceptors in juxtaglomerular apparatus near
renel glomerulus sense decreased blood flow .
It decreases the impulse generation in baroreceptors
which leads to the renin secretion.
Renin converts the angiotensin II into angiotensin I in
bloodstream which in lungs again converted into
angiotensin II in lungs.

36. It binds with angiotensin receptors on the blood
vessel causing vessel constriction thus increasing the
blood flow towards brain and heart to increase the
cardiac output.
 Vasopressin:
Vasopressin is released from the posterior pituitary
gland in response to decreased blood volume like
baroreceptors.
Vasopressin binds with VI receptors on arterioles
thus causing vasoconstriction

37.  It improves the vascular tone to maintain the
delivery of blood to the tissues.
 It also increases the return of blood towards the
heart and cardiac output is maintained.

38. If patient survives the shock situation, final stage
involves the replacement of blood volume. It takes
about 1 to 48 hours.
 Aldosterone:
At the same time, that angiotensin exerting effects
on blood vessels, it also stimulating adrenal glands
to secrete the aldosterone from adrenal cortex.
Aldosterone increases the Na absorption in DCT.
Water follows the Na and reabsorbed into blood
thus increasing the blood volume.

39.  Antidiuretic Harmone:
Vasopressin and ADH are the same harmones but
two names reflect two divergent functions.
So ADH harmone binds to V2 receptors in collecting
ducts of the kidney. This induces the insertion of
aquaporins channels into collecting ducts to allow
water reabsorption.
ADH also increases the thrist so that more water
intake and thereby increased blood volume and
venous return.

40. Thank