This document defines and describes various types of shock, including their causes, pathophysiology, clinical manifestations, and treatment. It discusses hypovolemic, cardiogenic, septic, and neurogenic shock. Hypovolemic shock results from loss of circulating blood volume from hemorrhage or fluid losses. Cardiogenic shock is caused by severe cardiac dysfunction. Septic shock involves systemic inflammation and hypotension due to infection. Neurogenic shock occurs when there is reduced sympathetic tone affecting blood vessels and the heart. The document provides details on the mechanisms, signs, and goals of treatment for each type of shock.

1. SHOCK
ABHISHEK PRAKASH
Roll no. 05
Para 15
Guided by
Dr . MUKESH RANA Sir
Dr . BRIJESH Sir
Dr . ASIF AKHTAR Sir
Dr . JAVED Sir
Dr . RAJESH Sir

2. Definition
Shock is a state in which diminished cardiac
output or reduced circulating blood volume
impairs tissue perfusion and leads to cellular
hypoxia.

3. Clinical shock is usually accompanied by
hypotension (i.e., a mean arterial pressure
[MAP] <60 mmHg in previously normotensive
persons).

4. Major types of shock

5. Pathogenesis and organ response
All forms of shock involve following 3
derangements:
Reduced effective circulating blood volume.
Reduced supply of oxygen to the cells.
Inflammatory mediators and toxins released
from shock induced cellular injury.

6. MICROCIRCULATION
Normally when cardiac output falls, systemic vascular
resistance rises to maintain a level of systemic
pressure that is adequate for perfusion of the heart
and brain at the expense of other tissues such as
muscle, skin, and especially the gastrointestinal (GI)
tract.
However, when MAP drops to ≤60 mmHg, blood flow
to these organs falls, and their function
deteriorates.

7. NEUROENDOCRINE RESPONSE
Hypovolemia, hypotension, and hypoxia are
sensed by baroreceptors and chemoreceptors
that contribute to an autonomic response that
attempts to restore blood volume, maintain
central perfusion, and mobilize metabolic
substrates.
Hypotension disinhibits the vasomotor center,
resulting in increased adrenergic output and
reduced vagal activity.

8. HYPOVOLEMIC SHOCK
The most common form of shock results either
from the loss of red blood cell mass and
plasma from hemorrhage or from the loss of
plasma volume alone due to extravascular
fluid sequestration or GI, urinary, and
insensible losses.

9. Pathophysiology of hypovolemic shock-
↓blood volume→ ↓venous return,→ ↓stroke
volume, ↓CO→ ↓BP

10. The normal physiologic response to
hypovolemia is to maintain perfusion of the
brain and heart while attempting to restore an
effective circulating blood volume. There is an
increase in sympathetic activity,
hyperventilation, release of stress hormones,
and an attempt to replace the loss of
intravascular volume through the recruitment
of interstitial and intracellular fluid and by
reduction of urine output.

12. TREATMENT
• Volume resuscitation is initiated with the rapid
infusion of either isotonic saline or a balanced salt
solution such as Ringer’s lactate through large-bore
intravenous lines.
• The infusion of 2–3 L of salt solution over 20–30
min should restore normal hemodynamic
parameters.

13. • Continuing acute blood loss with hemoglobin
concentrations declining to ≤100 g/L (10 g/dL)
should initiate blood transfusion preferably as fully
cross-matched, recently banked (<14 days old)
blood.
• Following severe and/or prolonged hypovolemia,
inotropic support with norepinephrine,
vasopressin, or dopamine may be required to
maintain adequate ventricular performance but
only after blood volume has been restored.

14. CARDIOGENIC SHOCK
Cardiogenic shock (CS) is characterized by
systemic hypoperfusion due to severe
depression of the cardiac index (<2.2
[L/min]/m2) and sustained systolic arterial
hypotension (<90 mmHg) despite an elevated
filling pressure (pulmonary capillary wedge
pressure [PCWP] >18 mmHg).

16. • Clinical findings
• Most patients have dyspnea and appear
pale, apprehensive and diaphoretic, and
mental status may be altered.
• The pulse is typically weak and rapid,
often in the range of 90–110 beats/min,
or severe bradycardia due to high-grade
heart block may be present.

17. • Laborartory findings
• The white blood cell count is typically
elevated with a left shift.
• Renal function is initially unchanged, but
blood urea nitrogen and creatinine rise
progressively.
• The lactic acid level is elevated.
• Cardiac markers, creatine phosphokinase
and its MB fraction, and troponins I and
T are typically markedly elevated.

18. Systolic BP
70 to 100 mmHg
NO signs/symptoms
of shock
Systolic BP
less than 100 mmHg
signs/symptoms of
shock

19. SEPTIC SHOCK
Sepsis with hypotension (arterial blood pressure
<90 mmHg systolic, or 40 mmHg less than
patient’s normal blood pressure) for at least 1 h
despite adequate fluid resuscitation
Need for vasopressors to maintain systolic blood
pressure ≥90 mmHg or mean arterial pressure
≥70 mmHg
or

20. Pathogenesis of septic shock

21. CLINICAL MANIFESTATIONS
• Disorientation, confusion, and other manifestations
of encephalopathy may also develop.
• Acrocyanosis and ischemic necrosis of peripheral
tissues (e.g., digits) due to hypotension and DIC
• Cellulitis, pustules, bullae, or hemorrhagic lesions
may develop when hematogenous bacteria or fungi
seed the skin or underlying soft tissue.

22. TREATMENT
• These measures should be initiated within 1 h
of the patient presentation with severe sepsis
or septic shock.
• Antimicrobial chemotherapy should be started
as soon as samples of blood and other
relevant sites have been obtained for culture.
• Removal or drainage of a focal source of
infection is essential.
• The primary goals are to restore adequate
oxygen and substrate delivery to the tissues as
quickly as possible and to improve tissue
oxygen utilization and cellular metabolism.

23. Numerous interventions have been tested for
their ability to improve survival rates among
patients with severe sepsis.
The list includes endotoxin-neutralizing proteins,
inhibitors of cyclooxygenase or nitric oxide
synthase, anticoagulants, polyclonal
immunoglobulins, glucocorticoids, a
phospholipid emulsion, and antagonists to
TNF-α, IL-1, platelet-activating factor, and
bradykinin.

24. NEUROGENIC SHOCK
Nervous system provides tone to blood vessels
and also to the heart and this tone is known
as Sympathetic tone.
The blood flow through the vascular system, it is
going to be maintained in forward direction by
the blood vessels because if it hits vessel wall
the blood vessels will bounce it back and
pushes the blood forward.

25. SYMPTOMS
Organ dysfunction
Bradycardia
Worm skin- dilation of blood vessel
TREATMENT
Vasopressors
IV fluid
Atropine

26. Physiologic Characteristics of the
Various Forms of
Shock
SHOCK CO SVR PCWP/LVEDV VENOUS O2
SATURATION
CARDIOGENIC ↓↓ ↑↑ ↑↑↑ ↓
HYPOVOLEMIC ↓ ↑↑↑ ↓ ↓
NEUROGENIC ↓ ↓ ͠ ↓
SEPTIC ↑ — ↓ ↓↓ ͠ ↓ ↑ or ↓

27. THANK
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