Guyton and Hall Chap 24

Chapter 24 Circulatory shock and its treatment

Wednesday, December 16, 2020

12:19 PM

Circulatory shock - generalized inadequate blood flow through the body, to the extent that the body tissues are damaged especially because of too little oxygen and nutrients are delivered to the tissue cells.

 

#Physiologic causes of shock

*circulatory shock caused by decreased cardiac output

Shock usually results from inadequate cardiac output.

1. Cardiac abnormalities that reduce the ability of the heart to pump blood

The circulatory shock resulting from diminished ability of the heart to pump blood: cardiogenic shock

1. Factors that decrease venous return

The most common cause Diminished blood volume

But also could be a result of decreased vascular tone especially of the venous reservoirs

Or obstruction to blood flow at some point in the circulation esp in the venous return pathway to the heart

*circulatory shock that occurs without diminished cardiac output

Occasionally even with the cardiac output that is normal or is even greater than normal, the person goes into a circulatory shock. Reasons.

1. Excessive metabolic rate so that even a normal cardiac output is inadequate
2. Abnormal tissue perfusion patterns so most of the cardiac output is not passing through the needy blood vessels

Inadequate delivery of nutrients to critical tissues and critical organs and also cause inadequate removal of wastes from the tissues.

*what happens to arterial pressure in circulatory shock?

Arterial pressure can be seriously misleading

A person in a severe shock might have normal arterial pressure because of powerful nervous reflexes at work

A person with normal perfusion might have a arterial pressure that has fallen by half

In most types of shock however, especially in case of severe blood loss, the arterial pressure and cardiac output decreases but arterial pressure does not fall as much as the cardiac output

*tissue deterioration is the end result of circulatory shock

Once circulatory shock reaches a critical state of severity, regardless of the initiating reason, the shock itself leads to more shock. Inadequate blood supply causes tissues to deteriorate and this affects the cardiac system as well causing more decreased cardiac output and so forth  a vicious cycle ensues

*stages of shock

1. Nonprogressive stage (compensated stage) - the normal circulatory compensatory mechanisms eventually cause full recovery without help from outside therapy
2. Progressive stage - without therapy shock progresses until death
3. Irreversible stage - no known treatment will be effective

 

 

#shock caused by hypovolemia - hemorrhagic shock

Hypovolemia - diminished blood volume. Hemorrhage, the most common cause

Hemorrhage decreases the filling pressure of the circulation and decreases venous return as a result

*relationship to bleeding volume to cardiac output and arterial pressure

About 10% of the blood can be removed with no effect on arterial pressure or the cardiac output.

But greater blood loss usually diminishes the cardiac output first then the arterial pressure.

Both arterial pressure and cardiac output reaches zero when about 40 to 45% of the blood has been removed.

-sympathetic reflex compensations in shock - their special value to maintain arterial pressure

Decrease in arterial pressure after hemorrhage as well as pressures in pulmonary arteries and veins in the thorax causes powerful sympathetic reflexes (arterial baroreceptors and other vascular stretch receptors) - stimulates vasoconstrictor system in most tissues of the body. Its effect:

1. Arterioles constrict in most parts of the body increasing the total peripheral resistance
2. Veins and venous reservoirs constrict, providing adequate venous return despite the decreased blood volume
3. Heart activity increases markedly raising the heart beat upto 160 to 180 beats/min.

-value of the sympathetic nervous reflexes

Without the sympathetic nervous reflexes, only 15 to 20 percent of the blood volume can be removed over a period of thirty minutes before a person dies compared to sustained life upto a 30 to 40 percent blood loss.

-greater effect of the sympathetic nervous reflexes in maintaining arterial pressure than in maintaining cardiac output

Arterial pressure is maintained at a normal level for a longer period than the cardiac output.

Usually this is done by increasing the total peripheral resistance. But this also constricts the veins and keeps the venous return volume up.

The second plateau in figure 24-1 is the activation of central nervous system ischemic response, the last ditch stand. Chap 18.

-protection of coronary and cerebral blood flow by the reflexes

*progressive and nonprogressive hemorrhagic shock

The circulatory system can recover as long as the degree of hemorrhage is no greater than a certain critical amount. Crossing this critical threshold by even a few mililiters of blood loss makes the difference between life and death. This means that a certain critical level causes shock to become progressive meaning shock causing more shock

-nonprogressive shock - compensated shock

The factors that cause a person to recover from moderate degrees of shock are negative feedback control mechanisms of the circulation that attempt to recover the arterial pressure and cardiac output to normal levels

1. Baroreceptor reflexes
2. Central nervous system ischemic response
3. Reverse stress-relaxation of the circulatory system
4. Increased secretion of renin by the kidneys and the formation of angiotensin2
5. Increased secretion by the post pituitary of vasopressin or antidiuretic hormone
6. Increased secretion by the adrenal medulla of norepinephrine and epinephrine
7. Compensatory mechanisms that return the blood volume back toward normal including large amounts of fluid absorption from the intestinal tract, absorption of fluid into the blood capillaries from the intestinal spaces  of the body, conservation of water and fluid by the kidneys, increased thirst and appetite for salt….

Within 30 seconds to a few minutes : sympathetic reflexes and increased secretion of catecholamines by the adrenal medullae

10minutes to an hour - angiotensin and vasopressin as well as reverse stress-relaxation that causes contraction of the blood vessels and venous reservoirs.

1 to 48 hours - readjustment of blood volume by absorption of fluid from intestinal sources and thirst mechanisms and more

-progressive shock is caused by a vicious circle of cardiovascular deterioration

• cardiac depression
• Vasomotor failure
• Blockage of very small vessels - sludged blood
• Increased capillary permeability
• Release of toxins by ischemic tissue
• Cardiac depression caused by endotoxin
• Generalized cellular deterioration
• Tissue necrosis in severe shock - patchy areas of necrosis occur because of patchy blood flows in different organs
• Acidosis in shock

-positive feedback deterioration of tissues in shock and the vicious circle of progressive shock

Not all positive feedbacks lead to a vicious cycle

*irreversible shock

Ironically, even in this irreversible stage, therapy can, on rare occasions, return the arterial pressure and even the cardiac output to normal or near normal for short periods, but the circulatory system nevertheless continues to deteriorate and death ensues in another few minutes to few hours.

-depletion of cellular high-energy phosphate reserves in irreversible shock

*hypovolemic shock caused by plasma loss

Loss of plasma without the loss of rbcs can cause hypovolemic shock similar to that caused by hemorrhage. Severe plasma loss occurs in intestinal obstruction, or severe burns or denuding skin conditions.

Plasma loss causes higher concentration of rbcs so as a result the viscosity of the blood thickens and causes sluggish blood flow.

1. Excessive sweating
2. Fluid loss in severe diarrhea or vomiting
3. Excess loss of fluid by the kidneys
4. Inadequate intake of fluid and electrolytes
5. Destruction of adrenal cortices with loss of aldosterone secretion and consequenst failure of the kidneys to reabsorb sodium, chloride and water which occurs in the absence of adrenocortical hormone aldosterone.

*hypovolemic shock caused by trauma

One of the most common causes of circulatory shock is trauma to the body. Often the shock results simply from hemorrhage caused by trauma, but it can also occur even without hemorrhage, because extensive contusion of the body can damage the capillaries sufficiently to allow excessive loss of plasma into the tissues.

 

#neurogenic shock - increased vascular capacity

Sometimes shock results because the vascular capacity increases so much that even the normal amount of blood  becomes incapable of filling the coronary system adequately.

One of the major cause for this is the sudden loss of vasomotor tone throughout the body, resulting esp. in massive dilation of the veins.

*causes of neurogenic shock

1. Deep general anesthesia
2. Spinal anesthesia
3. Brain damage is often a cause of vasomotor paralysis. Many patients who have had brain concussion or contusion of the basal regions of the brain develop profound neurogenic shock. Also prolonged ischemia causes total inactivation of the vasomotor neurons in the brain stem, with consequent development of severe neurogenic shock.

 

#anaphylactic shock and histamine shock

An allergic condition in which the cardiac output and arterial pressure often decrease drastically.

An antigen-antibody reaction that causes histamine release or a histamine like substance.

This causes

1. An increase in vascular capacity because of venous dilation, causing a marked decrease in venous return
2. Dilation of the arterioles, arterial pressure goes down
3. Greatly increased capillary permeability

Net effect: a great reduction in venous return and sometimes such serious shock that the person dies within minutes

 

#septic shock

"blood poisoning" a bacterial infection widely disseminated to many areas of the body, with the infection being borne through the blood from one tissue to another and causing extensive damage.

Septic shock is very important because other than the cardiogenic shock, septic shock is the most frequent cause of shock-related death in the modern hospital.

Some typical causes

1. Peritonitis caused by spread of infection from the uterus and fallopian tubes, sometimes resulting from instrumental abortion performed under unsterile conditions
2. Peritonitis resulting from rupture of the GI system, sometimes caused by intestinal disease and sometimes by wounds
3. Generalized bodily infection resulting from spread of a skin infection such as streptococcal or staphylococcal infection
4. Generalized gangrenous infection resulting from gas gangrene bacilli, spreading first through peripheral tissues and finally by way of the blood to the internal organs, esp the liver
5. Infection spreading into the blood from the kidney or urinary tract, often caused by colon bacilli

*special features of septic shock

1. High fever
2. Often marked vasodilation throughout the body, especially in the infected tissues
3. High cardiac output in perhaps half the patients caused by arteriolar dilation in the infected tissues and by high metabolic rate and vasodilation elsewhere in the body, resulting from bacterial toxin stimulation of cellular metabolism and from high body temperature
4. Sludging of blood, caused by red cell agglutination in response to degenerating tissues
5. Development of microblood clots in widespread areas of the body, a condition called disseminated intravascular coagulation. This causes clotting factors to be used up. So hemorrhaging occurs in many tissues, esp in the gut wall of the intestinal tract.

At the beginning only signs of infection but with time the circulatory system usually becomes involved either because of direct extension of the infection or secondarily as a result of toxins from the bacteria, with resultant loss of plasma into the infected tissues through deteriorating capillary walls. End  manifestations or the pathological steps do not differ greatly from hemorrhagic shock.

 

#physiology of treatment in shock

*replacement therapy

-blood and plasma transfusion

-dextran solution as a plasma substitute

*treatment of shock with sympathomimetic drugs - sometimes useful, sometimes not

Sympathomimetic drugs are drugs that mimics sympathetic stimulation like epinephrine, norepinephrine and more.

 in neurogenic shock and anaphylactic shock, these drugs help.

But in hemorrhagic shock it is not helpful because sympathetic nervous system is working at full measure

*other therapy

-treatment by the head-down position

Hemorrhagic shock and neurogenic shock, placing the head at least 12 inches below feet helps in promoting venous return. This is the first essential step in the treatment of many types of shock.

-oxygen therapy

Not as effective because it is the delivery of oxygenated blood that is mostly the problem

-treatment with glucocorticoids (adrenal cortex hormones that control glucose metabolism)

1. Experiments have shown empirically that glucocorticoids frequently increase the strength of the heart in late stages of shock
2. Glucocorticoids stabilize lysosomes in tissue cells and thereby prevent release of lysosomal enzymes into the cytoplasm of the cells, thus preventing deterioration from this source
3. Glucocorticoids might aid in the metabolism of glucose by the severely damaged cells

 

#circulatory arrest

All blood flow stops

Usually as a result of cardiac arrest or ventricular fibrillation

*effect of circulatory arrest on the brain

5 to 8 minutes of total circulatory arrest can cause at least some degree of permanent brain damage in more than half of patients. 10 to 15 minutes almost always permanently destroys significant amounts of mental power.

Through experiment it is known that rather than lack of oxygen, it is the blood clots that was more the immediate issue. The clots likely block the small vessels, leading to prolonged ischemia and eventual death of the neurons. Without blood 30 minutes passed before permanent brain damage and heparin or streptokinase before cardiac arrest was shown to increase the survivability of the brain upto two to four times longer than usual.