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Phys Ch 24
Physiologic Causes of Shock
 Circulatory shock – generalized inadequate blood flow through body to extent that body tissues are damaged
o Once cardiovascular system itself (heart, walls of blood vessels, etc.) is affected by shock, vicious cycle of
shock gets worse
 Shock usually results from inadequate cardiac output – any condition that reduces cardiac output far below
normal leads to shock
o Cardiac abnormalities that decrease ability of heart to pump blood – MI, toxic states of heart, severe
heart valve dysfunction, heart arrhythmias – any of these would be cardiogenic shock
o Factors that decrease venous return – decrease cardiac output because heart cannot pump blood it
doesn’t get – most common cause is diminished blood volume, but venous return can also be reduced
because of decreased vascular tone or obstruction to blood flow
 Cardiac output can be normal or greater than normal and person still goes into shock
o Excessive metabolic rate, so even normal cardiac output is inadequate
o Abnormal tissue perfusion patterns, so most of cardiac output is passing through blood vessels besides
those that supply local tissues with nutrition
 Person can be in severe shock and have almost normal arterial pressure because of powerful nervous reflexes
that keep pressure from falling
o Other times person can have very low arterial pressure and still not be in shock (have normal tissue
perfusion)
o In most types of shock, especially hypovolemic shock, arterial blood pressure decreases at same time
cardiac output decreases, though usually not as much
 Once circulatory shock reaches critical state of severity, regardless of its cause, shock leads to more shock
o Inadequate blood flow causes body tissues to deteriorate, including heart and circulatory system,
causing even greater decrease in cardiac output, and vicious cycle ensues
 Stages of shock – change with degrees of severity
o Nonprogressive stage (compensated stage) – normal circulatory compensatory mechanisms eventually
cause full recovery without outside help
o Progressive stage – tipping the scales into the vicious cycle (without help, they will die)
o Irreversible stage – shock has progressed to such an extent that all forms of known therapy are
inadequate to save the person’s life, even though they are still alive (for the moment)
Shock Caused by Hypovolemia – Hemorrhagic Shock
 Hypovolemia – diminished blood volume
 Hemorrhage is most common cause of hypovolemic shock – decreases filling pressure of circulation and thus
decreases venous return
 Cardiac output and arterial pressure fall to zero when 40-45% of total blood volume removed (in 30 minutes)
 Decrease in arterial pressure after hemorrhage, as well as decreases in pressures in pulmonary arteries and
veins, cause powerful SNS reflexes (initiated mainly by arterial baroreceptors and other vascular stretch
receptors) – stimulate SNS vasoconstrictor system in most tissues of body, resulting in
o Arterioles constrict in most parts of systemic circulation, increasing total peripheral resistance
o Veins and venous reservoirs constrict, helping maintain adequate venous return despite diminished
blood volume
o Heart activity increases markedly, increasing heart rate
 In absence of reflexes, only 15-20% of blood volume can be removed over period of 30 minutes before person
dies (1/2 the amount that one can usually lose before death is imminent)
 Arterial pressure maintained at or near normal level longer than cardiac output in hemorrhaging person because
SNS reflexes are geared more for maintaining arterial pressure than for maintaining cardiac output – increase
arterial pressure mainly by increasing total peripheral resistance, which has no benefit on cardiac output
o SNS constriction of veins is important to keep venous return and cardiac output from falling too much
o Second plateau occurs in arterial pressure around 50 mm Hg because of activation of CNS ischemic
response, which causes extreme stimulation of SNS when brain begins to suffer from lack of oxygen or
from excess buildup of CO2 – called the “last-ditch stand” of SNS reflexes to keep arterial pressure from
falling too low

Maintenance of normal arterial pressure even in presence of decreasing cardiac output protects blood flow
through coronary and cerebral circulatory systems
o SNS stimulation does not cause significant constriction of either cerebral or cardiac vessels
o In both cerebral and cardiac vascular beds, local blood flow autoregulation is excellent, which prevents
moderate decreases in arterial pressure from significantly decreasing blood flow
o Because of above, blood flow through heart and brain is maintained essentially at normal levels as long
as arterial pressure doesn’t fall below about 70 mm Hg (blood flow in some other areas of body might
be decreased to as little as 1/3-1/4 normal by this time because of vasoconstriction
 Circulatory system can recover as long as degree of hemorrhage is no greater than a certain critical amount –
crossing this critical threshold, even by a few mL, makes eventual difference between life and death
o Hemorrhage beyond a certain critical level makes shock become progressive, leading to deterioration of
circulation and death
 Factors that cause person to recover from moderate degrees of shock are all negative feedback control
mechanisms of circulation that attempt to return cardiac output and arterial pressure back to normal levels
o Baroreceptor reflexes – elicit powerful SNS stimulation of circulation
o CNS ischemic response – elicits even more powerful SNS stimulation throughout body, but not activated
significantly until arterial pressure below 50 mm Hg
o Reverse stress-relaxation of circulatory system, which causes blood vessels to contract around
diminished blood volume so blood volume that is available more adequately fills circulation
o Increased secretion of renin by kidneys and formation of angiotensin II, which constricts peripheral
arteries and causes decreased output of water and salt by kidneys
o Increased secretion of ADH by posterior pituitary gland – constricts peripheral arteries and veins and
greatly increases water retention by kidneys
o Increased secretion of epinephrine and norepinephrine – constricts peripheral arteries and veins and
greatly increases water retention by kidneys
o Compensatory mechanisms that return blood volume back toward normal, including absorption of large
quantities of fluid from intestinal tract, absorption of fluid into blood capillaries from interstitial spaces
of body, conservation of water and salt by kidneys, and increased thirst and increased appetite for salt
 SNS reflexes and increased secretion of catecholemines by adrenal medullae provide rapid help toward bringing
about recovery because they become maximally activated within 30 seconds to a few minutes after hemorrhage
 Angiotensin and vasopressin (ADH) mechanisms and reverse stress-relaxation require 10 minutes to an hour to
respond completely, but aid greatly in increasing arterial pressure or increasing circulatory filling pressure and
thereby increasing return of blood to heart
 Readjustment of blood volume by absorption of fluid from interstitial spaces and intestinal tract, as well as oral
ingestion and absorption of additional water and salt, may require 1-48 hours
Progressive Hypovolemic Shock
 When arterial pressure falls low enough, coronary blood flow decreases below that required for adequate
nutrition of myocardium, weakening heart muscle and thereby decreasing cardiac output more
 Deterioration of heart isn’t obvious in early stages of shock because deterioration of heart is not severe yet as
well as because heart has tremendous reserve capability that normally allows it to pump more blood than
normal
 In latest stages of shock, deterioration of heart is most important factor in final lethal progression of shock
 In early stages of shock, various circulatory reflexes cause intense activity of SNS, but eventually diminished
blood flow to brain’s vasomotor center depresses the center so much that it becomes progressively less active
and finally totally inactive
o Complete circulatory arrest to brain causes most intense of all SNS changes during first 4-8 minutes, but
by end of 10-15 minutes, vasomotor center becomes so depressed that there is no more SNS reaction
o Vasomotor center usually does not fail unless arterial pressure drops below 30 mm Hg
 Many small blood vessels get blockage from sluggish blood flow through microvessels – because tissue
metabolism continues despite low flow, large amounts of carbonic and lactic acid continue to empty into local
blood vessels and greatly increase local acidity of blood – acid plus other deterioration products from ischemic
tissues cause local blood agglutination, resulting in minute blood clots, leading to very small plugs in small
vessels
o
Increased tendency for blood cells to stick to one another make it more difficult for blood to flow
through microvasculature, giving rise to “sludged blood”
 After many hours of capillary hypoxia and lack of nutrients, permeability of capillaries gradually increases, and
large quantities of fluid begin to transude into tissues, decreasing blood volume even more, decreasing cardiac
output, making shock still more severe – not until late stages of prolonged shock
 Significant shock releases endotoxin in some types of shock – released from bodies of dead gram-negative
bacteria in intestines
o Diminished blood flow to intestines causes enhanced formation and absorption of endotoxin
o Circulating endotoxin causes increased cellular metabolism despite inadequate nutrition of cells, causing
cardiac depression
o Plays an important role in septic shock
 Liver is affected in shock because of lack of enough nutrients to support normally high rate of metabolism in
liver cells, but partly because of exposure of liver cells to any vascular toxin or other abnormal metabolic factor
occurring in shock
 Damaging cellular effects in most body tissues include
o Active transport of Na+ and K+ through cell membrane greatly diminished, allowing Na+ and Cl- to
accumulate in cells and K+ is lost from cells – some cells begin to swell
o Mitochondrial activity in liver cells and many other tissues of body become severely depressed
o Lysosomes in cells begin to break open, with intracellular release of hydrolases that cause further
intracellular deterioration
o Cellular metabolism of nutrients, such as glucose, eventually becomes greatly depressed in last stages of
shock – actions of some hormones depressed as well, including almost 100% depression of insulin
 Deterioration of organs of body especially bad in
o Liver – depression of metabolic and detoxification functions
o Lungs – eventual development of pulmonary edema and poor ability to oxygenate blood
o Heart – further depressing contractility
 Not all cells of body are equally damaged by shock because some tissues have better blood supplies than others
o Cells adjacent to arterial ends of capillaries receive better nutrition than cells adjacent to venous ends of
same capillaries, so more nutritive deficiency occurs around venous ends of capillaries than elsewhere
o Punctate lesions occur in heart muscle, playing an important role in leading to final irreversible stage
o Deteriorative lesions occur in liver and kidneys – leads to kidney failure and uremic death several days
later; necrosis in center of liver lobules (last exposed to blood as it passes through liver sinusoids)
o Deterioration of lungs often leads to respiratory distress and death (shock lung syndrome)
 Most metabolic derangements that occur in shocked tissue lead to acidosis all through body
o Lactic acid and carbon dioxide build up in tissues
o Acidosis leads to further progression of shock itself
 Positive feedback loops themselves don’t necessarily start the vicious cycle; depends on the intensity
Irreversible Shock
 After a certain point, transfusion and treatment can restore cardiac output and arterial pressure, but patient still
dies – by this time, multiple deteriorative changes have occurred in heart that may not necessarily affect its
immediate ability to pump blood but, over a long period, depress heart pumping enough to cause death
o Tissue damage, release of destructive enzymes, acidosis, and all the other factors are too much
 High energy phosphate reserves, especially in liver and heart, get used up – almost all creatine phosphate has
been degraded and almost all ATP converted to ADP, AMP, and adenosine (much of adenosine diffuses out and
is converted to uric acid, and ATP is reformed very slowly, so it would take too long to recreate needed amount)
o Loss of ATP is most significant for development of irreversibility
Hypovolemic Shock Caused by Plasma Loss
 Severe plasma loss can occur from
o Intestinal obstruction – distention of the intestine in intestinal obstruction partly blocks venous blood
flow in intestinal walls, increasing intestinal capillary pressure, which causes fluid to leak from capillaries
into intestinal walls and intestinal lumen; because lost fluid has high protein content, total blood plasma
protein is reduced, and thus plasma volume is reduced
o
In patients with severe burns or other denuding conditions of skin, so much plasma is lost through
denuded skin areas that plasma volume becomes markedly reduced
 Has almost same characteristics as hemorrhagic hypovolemic shock, plus blood viscosity increases greatly as a
result of increased RBC concentration, which exacerbates sluggishness of blood flow
 Dehydration (loss of fluid from all body compartments) can reduce blood volume and cause hypovolemic shock
o Can be caused by excessive sweating, fluid loss from severe vomiting or diarrhea, excess loss of fluid
from kidneys, inadequate intake of fluid and electrolytes, or destruction of adrenal cortices (loss of
aldosterone secretion and consequent failure of the kidneys to reabsorb Na, Cl, and water because of
loss of aldosterone)
Hypovolemic Shock Caused by Trauma
 Can happen from hemorrhage, but can also happen because extensive contusion can damage capillaries
sufficiently to allow excessive loss of plasma into tissues, resulting in reduced plasma volume (hence shock)
 Mostly hypovolemic shock, but also can have moderate degree of neurogenic shock caused by loss of vasomotor
tone
Neurogenic Shock
 Vascular capacity increases so much that even normal amount of blood becomes incapable of filling circulatory
system adequately – one of major causes is sudden loss of vasomotor tone throughout body, resulting especially
in massive dilation of veins
 Either an increase in vascular capacity or a decrease in blood volume reduces mean systemic filling pressure,
which reduces venous return
 Diminished venous return caused by vascular dilation is called venous pooling
 Neurogenic factors that can cause loss of vasomotor tone include
o Deep general anesthesia – often depresses vasomotor center enough to cause vasomotor paralysis, with
resulting neurogenic shock
o Spinal anesthesia, especially when this extends all the way up the spinal cord, blocks SNS nervous
outflow from nervous system and can be a potent cause of neurogenic shock
o Brain damage – many patients who have had brain concussion or contusion of basal regions of brain
develop profound neurogenic shock; even though brain ischemia for a few minutes almost always
causes extreme vasomotor stimulation, prolonged ischemia (longer than 5-10 min) can cause total
inactivation of vasomotor neurons in brain stem, with consequent development of severe neurogenic
shock
Anaphylactic Shock and Histamine Shock
 Cardiac output and arterial pressure often decrease drastically; results primarily from antigen-antibody reaction
that rapidly occurs after antigen to which the person is sensitive enters circulation
 Basophils and mast cells released in the pericapillary tissues, and they release histamine and histamine-like
substances that
o Increase vascular capacity because of venous dilation, thus causing a marked decrease in venous return
o Dilate arterioles, resulting in greatly reduced arterial pressure
o Greatly increase capillary permeability, with rapid loss of fluid and protein into tissue spaces
 Net effect is great reduction of venous return
 Histamine shock – anaphylactic shock caused by overinjection of histamine
Septic Shock
 Bacterial infection widely disseminated to many areas of body, with infection being borne through blood from
one tissue to another, causing extensive damage
 Second most common cause of shock-related death in modern hospital (second to cardiogenic shock)
 Typical causes of septic shock
o Peritonitis caused by spread of infection from uterus and fallopian tubes, sometimes resulting from
instrumental abortion performed under unsterile conditions
o Peritonitis resulting from rupture of GI system, caused by intestinal disease or wounds
o Generalized bodily infection resulting from spread of bacterial skin infection
o Generalized gangrenous infection resulting specifically from gas gangrene bacilli, spreading first through
peripheral tissues and finally by way of blood to internal organs, especially the liver
o Infection spreading into blood from kidney or urinary tract, often caused by colon bacilli
 Common symptoms include high fever, vasodilation throughout body (especially in infected tissues), high
cardiac output caused by arteriolar dilation in infected tissues and high metabolic rate and vasodilation
elsewhere in body resulting from bacterial toxin stimulation of cellular metabolism and high body temperature,
sludging of blood caused by red cell agglutination in response to degenerating tissues, development of microblood clots in widespread areas of body (disseminated intravascular coagulation) which causes blood clotting
factors to be used up, so hemorrhaging occurs in many tissues, especially in gut wall of intestinal tract
 In early stages, patient shows signs of bacterial infection, but not circulatory collapse
 As infection becomes worse, circulatory system usually becomes involved either because of direct extension of
infection or secondarily as a result of toxins from bacteria, with resultant loss of plasma into infected tissues
through deteriorating blood capillary walls
 End stages of septic shock are similar to other forms of shock (including vicious cycle), even though start was
different
Physical Treatment of Shock
 If caused by hemorrhage, transfusion of whole blood helps; if caused by loss of plasma, plasma transfusion
helps; if caused by dehydration, IV fluids and electrolytes help
o Plasma can usually substitute adequately for whole blood because it increases blood volume and
restores normal hemodynamics
o Plasma cannot restore a normal hematocrit, but human body can usually stand decrease in hematocrit
to ½ of normal before serious consequences result (if cardiac output adequate)
 If plasma unavailable, plasma substitutes such as dextran solution can be used
o Principal requirement of truly effective plasma substitute is that it remain in circulatory system (does
not filter through capillary pores into tissue spaces)
o Must contain appropriate electrolytes to prevent derangement of body's extracellular fluid electrolytes
o To remain in circulation, plasma substitute must contain some substance that has large enough
molecular size to exert colloid osmotic pressure – dextran is large polysaccharide polymer of glucose
o Certain bacteria secrete dextran as by-product of growth, and commercial dextran can be manufactured
using bacterial culture procedure (molecular weight can be controlled by varying bacteria growth
conditions)
 Sympathomimetic drugs – mimic SNS stimulation; can use epinephrine, norepinephrine, and other long-acting
drugs that have same effects
o Works with neurogenic shock because SNS is depressed, and drugs take the place of diminished SNS
actions and can often restore full circulatory function
o Works with anaphylactic shock because sympathomimetic drugs have a vasoconstrictor effect that
opposes vasodilating effect of histamine
o Doesn’t work with hemorrhagic shock because SNS is already very activated
 Placing patient with head at least 12” lower than feet helps in promoting venous return, thereby also increasing
cardiac output
 Because major deleterious effect of most types of shock is too little delivery of oxygen to tissues, giving patient
oxygen can be of benefit, but not always effective because most times, lack of oxygen is due to inadequate
transport of blood after it is oxygenated
 Glucocorticoids are frequently given to patients in severe shock
o Glucocorticoids frequently increase strength of heart in late stages of shock
o Glucocorticoids stabilize lysosomes in tissue cells and thereby prevent release of lysosomal enzymes
o Glucocorticoids might aid in metabolism of glucose by severely damaged cells
Cardiac Arrest
 Cardiac arrest – when all blood flow stops, usually as a result of cardiac arrest or ventricular fibrillation
 May result from too little oxygen in anesthetic gaseous mixture or from depressant effect of anesthesia itself
 Normal cardiac rhythm can be restored by removing anesthetic and applying CPR measures (giving patient
oxygen ventilation)
 More than 5-8 min of total circulatory arrest can cause at least some degree of permanent brain damage in
more than half of patients; circulatory arrest for as long as 10-15 min almost always permanently destroys
significant amounts of mental power
o
o
o
If blood clots are prevented from occurring in brain blood vessels, this will also prevent much of early
deterioration of brain during circulatory arrest
Administration of heparin or streptokinase before cardiac arrest was shown to increase survivability of
brain 2-4x longer than usual
Severe brain damage that occurs from circulatory arrest is caused mainly by permanent blockage of
many small blood vessels by blood clots, thus leading to prolonged ischemia and eventual neuron death