Shock,

Cardiovascular collapse
?????????????????????????

SHOCK?
WHAT IS TYPES CF
 DEATH
SHOCK
• Microbial sepsis.
• Large myocardial infarction, SHOCK
• Massive pulmonary embolism, and
• Severe hemorrhage, SHOCK
• Extensive trauma or burns,
FINAL COMMON PATHWAY
Regardless of the underlying
pathology, shock gives rise to systemic
hypo perfusion; it can be caused
either by reduced cardiac output or by
reduced effective circulating blood
volume.
 Definition

 Is a state /failure of the circulatory

system to maintain adequate cellular
perfusion resulting in widespread
reduction in delivery of oxygen &other
nutrients to tissues.
Pa<60mmHg, PS<90mmHg
Classification of shock

A. Hypovolumic shock
B. Cardiogenic shock
C. Distributive shock
 Septic shock
 Neurogenic shock
 Anaphylactic shock
A. Hypovolumic shock

 Most common shock in clinical medicine.

 Loss of >25% of blood volume shock .

Definition: shock due to reduced blood volume

CO tissue perfusion.
Causes:
1. Haemorrhage
2. Diarrhea & vomiting
3. Trauma, burns, etc....
B. Cardiogenic shock

Definition: shock results from sever

depression of cardiac performance.
 Primarily-Pump failure (myocardial
failure)
 Hemodynamically defined as
 DBP<60mmHg
 Usually pulmonary edema coexists.
CAUSE
1. Myopathic
a. Acute MI-If >40% Left Ventricle &more on

Right ventricle infarction.

b. Myocarditis
c. Cardiomyopaties
d. Myocardial depression in septic shock
2. Mechanical obstruction
I. Intracardiac
 a. Out flow obstruction- E.g. -AS
 b. Arrhythmia
 c .Reduction in forward CO.
E.g. -AR, MR
II. Extra cardiac
Obstructive shock
 a. Pericardial tamponade
 b. Tension pneumothorax
 c. Acute severe PTE (50-60%
pulmonary bed involved)
 d. Sever pulmonary HTN(10)
SEPTIC SHOCK

 Mortality rate-25%-50%.
 First cause of death in ICU.
 Increasing incidence.
 Result from expansion of an initially
localized infection.
Causes
 >70% by endotoxin producing gram –ve
bacilli(Endotoxic shock)
 Gram +ve bacteria
Eg-Toxic shock syndrome.
 Fungi
Aspects of sepsis(terms):
 Bacteremia-Presence of viable bacteria in the
blood as evidenced by blood culture.
 Septicemia- Systemic infection due the
presence of microbes &their toxin in the
blood.
 Sepsis-A systemic response to sever infection
mediated via macrophage derived cytokines
that target end organ receptors in response to
infection SIRS / Systemic Inflammatory
Response Syndrome.
Pathogenesis
 Free LPS/ Lipo polysaccharide/bind with
circulating LPS binding protein.
 The complex bind to a cell surface
receptor(CD14).
 LPS bind to mammalian Toll- like receptor
(TLR-4.)
 Signal from TLR-4 directly activate
leukocytes and vascular wall cells.
 Initiate a cascade of cytokine mediators.
On epithelial cells
 Down regulation of natural anticoagulant
mechanisms.
On monocytes and macrophages
 Mononuclear cell activation.
 Subsequent production of potent effector
cytokines( IL1, TNF).
STAGES OF SHOCK

Uncorrected shock passes three stages:

1. Initial non-progressive phase.
2. Progressive stage (established shock)
3. An irreversible stage.
1. Non-progressive phase
Compensatory period  compensatory mechanisms activated
&perfusion of vital organs maintained
Mechanism:
 Neurohumeral mechanisms
CO  sympathoadrenal stimulationepinephrine
tachycardiaCO+
peripheral vasoconstrictionBP Major auto compensatory
response.
 Rennin aldosterone mechanism (RAAS)Renal conservation of
fluid.
2. Progressive stage
 Characterized by tissue hypo perfusion
with worsening of circulatory &
metabolic imbalances including acidosis.
 Wide spread tissue hypoxia.
 Anaerobic glycolysisexcessive lactic
acid production
 Anoxic injuryendothelial injuryDIC
 Clinically pt may become confused and
UOP declines.
3. An irreversible stage
 Stage at which if hemodynamic disorders
are corrected survival is not possible.
 This is mediated via various mechanisms.
 Widespread cell injury.
 Ischemic bowel.
 Complete renal shutdown.
Morphology of septic shock
 All organs affected.
 Widespread tissue hypo perfusion.
 Hypoxia tissue necrosis MODs/ Multi
Organ Dysfunction
 Brain-Develop ischemic encephalopathy.
 The heart - Coagulative necrosis.
 Kidney-Extensive tubular ischemic injury.
 Lungs- Diffuse alveolar damage(shock lung)
 Adrenalin-Cortical cell lipid depletion.
 GI-Patchy mucosal haemorrhage and
necrosis-hemorrhagic enteropathy.
 Liver-Fatty changes and central
haemorrhage necrosis.
Clinical course of shock
 Hypotension,
 Weak rapid pulse (HR),
 Tachypenia,
 Cool clammy extremities, cyanotic skin.
 CNS-confusion ,restlessness ,comma
death
 Kidneys-decrease urine out put –renal
failure-death
prognosis

 80-90% of young otherwise health

patients recover from hypovolumic
shock if appropriately managed.
 Mortality rate /MR reach 75% in
patients with Cardiogenic shock from
large MI or G- negative septic shock.
AMESEGINALEHU