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4/24/2013 Dr. Khaled Al-Qudah 1

Cardiovascular Shock

Dr. Khaled M. Al-Qudah


Shock is basically circulatory collapse.

It is constitutes widespread hypo-perfusion

of tissues due to reduction in the blood

volume or cardiac output, or redistribution

of blood, resulting in an inadequate

effective circulating volume.


There is insufficient delivery of oxygen

and nutrients to the cells and tissues and

inadequate clearance of waste products.

The cellular hypoxia results in anaerobic

metabolism, resulting in increased lactic

acid production. If the derangement is not

corrected, death of the cells and patient

occurs.


Major Classifications of shock

There are four major classifications of shock:

•Cardiogenic

•Hypovolemic

•Obstructive

•Vasogenic Distributive:

anaphylactic shock

neurogenic shock

septic shock


Cardiogenic shock:

Acute reduction of cardiac out put, due

to either:

valvular or myocardial disease

cardiac arrhythmia

myocardial depression associated with

drugs, toxins, or endogenous humoral

mediators


Hypovolemic shock

the volume of circulating fluid is significantly reduced.

absolute hypovolemia: results from the

loss of fluid from the vasculature; common

causes include: internal or external blood

loss, extravasation of fluid through

"leaky"endothelium, severe dehydration


Severe hemorrhage with loss of 35% or more of total blood volume.

[severe diarrhea

Dehydration [intestinal obstruction

[severe vomiting


relative hypovolemia:

results from inadequate vascular tone or

vasodilation; examples include:

Sepsis

Anaphylaxis


Vasogenic or distributive shock

inappropriate partitioning of blood flow so

that some tissues are hypo-perfused and

other areas hyper-perfused; loss of normal

vascular reactivity; loss of metabolic or

pressure autoregulation of blood flow

vascular abnormalities failure of the

distribution of the fluid


Causes of Vasogenic or distributive shock

severe trauma

widespread superficial burn

extensive surgery - considerable exposure and handling of the intestines

prolapse of the uterus.

sudden reduction of pressure in a body cavity; e.g. rapid withdrawal of ascitic fluid.

severe pain - equine colic.


Anaphylactic Shock

Anaphylactic shock occurs when an individual has

a severe allergic reaction to any substance. This

allergic reaction may result in massive

vasodilation and subsequent decreased cardiac

output.

Common causes of anaphylactic shock include

medications (i.e. penicillin, cephalosporins,

aspirin), bee stings, iodine based dyes.


Anaphylactic Shock…..

When an individual is re-exposed to a particular

substance, the antigen binds to immunoglobulin

located on the mast cells. This process causes the

release of chemicals from the cells, including

histamine, kallikrein and platelet-activating

factor. These chemicals cause massive

vasodilation, urticaria, laryngeal edema and

bronchoconstriction. Individuals suffering from

anaphylactic shock will die if untreated.


Toxic or septic shock:

Most cases of septic shock are caused by

gram-negative bacteria. Gram-negative

bacteria have walls composed of

lipopolysaccharides (LPS) or endotoxins.

All of the hemodynamic and metabolic

alterations of septic shock can be produced

by injections of LPS


LPS binds to receptors on leukocytes,

endothelial cells, and other cell types

inducing its effects in two ways:

• Directly, by causing injury to the function of

cells

• Indirectly by initiating the synthesis, release,

or activation of a cascade of mediators derived

from plasma and cells.

Toxic or septic shock….


These mediators affect a large number of vital

organ systems, including:

Heart (myocardial dysfunction)

Vascular system (vasodilation and hypotension)

Microcirculation (endothelial injury and leukocyte adhesion)

Coagulation (DIC)

Lungs (respiratory distress),

Liver (liver failure)

Kidneys (acute renal failure),

CNS (resulting in lethargy or coma).


Neurogenic Shock

Neurogenic shock is often caused by spinal

cord injury, which damages the ability of

the central nervous system to control

vessel dilation and constriction.

The most common spinal cord injuries

resulting in neurogenic shock involve

damage to the cervical spine area.


Obstructive Shock

a. gross obstruction: impedance of blood

flow in a major blood vessel or to a

particular organ/region; common

examples:

Vena cava obstruction

Pericardial fluid compromising venous

return

Thromboembolic disease


Obstructive Shock….

b. Microscopic obstruction :

Disruption in blood flow in the

microvascular environment; for example

disseminated intravascular coagulation


Physiology of Cardiovascular Shock

A decrease in effective circulating volume

results in decreased cardiac filling and cardiac

output.

The early physiologic responses include the

baroreceptor reflex. Baroreceptors present at

the aortic arch and carotid sinus detect a

decrease in arterial blood pressure and send

impulses to the brain stem via the afferent

buffer nerves in order to stimulate a sympatho-

adrenal response.


The release of norepinephrine directly

from nerve terminals innervating the

heart and blood vessels and the release of

epinephrine from the adrenal glands

cause an:

increase in venous tone (increased cardiac

filling)

increase in arterial tone (increased blood

pressure)

increase in cardiac output (increased heart

rate and contractility).


Arterial vasoconstriction occurs primarily

in skin, muscle, and visceral organs to

preferentially support coronary and

cerebral perfusion.

The baroreceptor response and ischemic

response of the brain are the most potent

reflexes to maintain blood flow to the two

most important organs: heart and brain.


Therefore blood pressure is usually the last to go in the context of hypovolemic shock. (i.e. a normal arterial blood pressure does not denote normal perfusion)

Intermediate term adaptations to the shock syndrome include a fluid flux from the interstitium into the intravascular space.


Decreased chloride delivery to the distal

nephron (to decreased GFR) results in

activation of the renin-angiotensin-

aldosterone system.

This initiates reduced GFR, decreased

urine output, conservation of sodium and

water, and global vasoconstriction.


Although ADH is usually more important in

the regulation of plasma osmolarity,

severe hypovolemia will result in ADH

release, conservation of water at the

collecting tubule of the kidney and intense

vasoconstriction.


The release of catecholamines and cortisol

increase the production of glucose via

glycogenolysis and luconeogenesis in an

attempt to support energy metabolism.

These changes are typical of the

hypovolemic model of compensated

cardiovascular shock.


If the shock syndrome continues or is not

treated, sympathetic stimulation becomes

more intense and leads to

vasoconstriction to a level that

compromises oxygen delivery to vital

organs in an effort to maintain coronary

and cerebral perfusion.


Oxygen uptake becomes maximal at the

compromised tissues and anaerobic

metabolism becomes necessary to support

cellular function.

Release of vasoactive substances such as

prostaglandins, leukotrienes, thromboxanes,

interleukins, among many others leads to mal-

distribution of blood flow (areas of intense

vasoconstriction and vasodilation), myocardial

depression, and activation of the clotting

cascade.


The terminal or decompensatory stages of

shock are similar regardless of the

etiology.

Prolonged sympathetic overactivity leads

to severe tissue hypoxia and acidosis, and

finally failure of the heart and brain (as

well as kidneys, liver, lungs,

gastrointestinal tract).


The heart rate slows or becomes

arrhythmic, peripheral veins and arteries

dilate, further decreasing venous return,

cardiac output, and arterial pressure.

Cardiopulmonary arrest occurs.


Clinical Findings

coldness of the skin

subnormal temperature

rapid shallow breathing

rapid heart rate

weak pulse of small amplitude and low pressure

pale gray m.m

capillary refill time is extended beyond 3-4 second

the animal is dull, weak, often recumbent


Necropsy finding:

No specific findings for shock, in all cases

there may be widespread evidence of

petechial and ecchymotic hemorrhage as a

result of Disseminated intravascular

coagulation” (DIC).


Treatment

The aim is to restore the circulating volume.

Blood transfusion

Plasma transfusion

Isotonic fluids


Vasoactive agents [ Pitressin ]: Very dangerous

unless the patient’s cardiovascular status can

be continually monitored.

-adrenergic stimulators [ Isoproterenol ] used

as vasodilators, once the circulating blood

volume has been restored, but if hypotension is

already present it will by further exacerbated


Glycocorticoids and antibiotics in case of Septic shock

Keeping the animal warm, also avoid overheating because it cause peripheral vasodilatation

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