Physiology of Cardiovascular shock.

CARDIOVASCULAR SHOCK
PRESENTER:DR MTONGWE
FACILITATOR: DR.F. BUKACHI

2
•Definition
•Basic Physiology
•Classification
•Causes
•Symptoms and Sings
•Treatment
•complication

DEFINITION
• generalized inadequate blood flow, to the
extent that the body tissues are damaged,
especially because too little oxygen and other
nutrients delivered to the tissue cells. Even
the cardiovascular system itself- the heart
musculature, walls of the blood vessels,
vasomotor system and other circulatory parts
begin to deteriorate. So shock, once begun, is
prone to become progressively worse.

DEFINITION
• Profound hemodyamic and metabolic
disturbance characterized by failure of the
circulatory system to maintain adequate
perfusion of vital organs

Physiological causes of shock.
• Circulatory shock caused by decreased cardiac
output.
• Shock usually results from inadequate cardiac out
put. Two types of factors reduce this:
1. Cardiac abnormality that decrease the ability of
the heart to pump blood- these include
myocardial infarction, toxic states of the heart,
valve dysfunction, arrhythmias etc
2. Factors that reduce the venous return. Eg
diminished blood vol. decreased vascular tone,
obstruction to the blood flow

Circulatory shock that occur without
diminished blood cardiac output
Occasionally, cardiac output is normal or even
greater than normal, yet the person is in
circulatory shock. This can result from (1)
excessive metabolic rate, so even a normal
cardiac output is inadequate, or (2) abnormal
tissue perfusion patterns, so most of the
cardiac output is passing through blood
vessels besides those that supply the local
tissues with nutrition.

• What Happens to the Arterial Pressure in Circulatory
Shock?
• In the minds of many physicians, the arterial pressure
level is the principal measure of adequacy of
circulatory function. However, the arterial pressure can
often be seriously misleading. At times, a person may
be in severe shock and still have an almost normal
arterial pressure because of powerful nervous reflexes
that keep the pressure from falling. At other times, the
arterial pressure can fall to half of normal, but the
person still has normal tissue perfusion and is not in
shock.

• In most types of shock, especially shock
caused by severe blood loss, the arterial blood
pressure decreases at the same time the
cardiac output decreases.

Tissue Deterioration Is the End Result
of Circulatory Shock
• Once circulatory shock reaches a critical state of
severity, regardless of its initiating cause, the shock
itself leads to more shock. That is, the inadequate
blood flow causes the body tissues to begin
deteriorating, including the heart and circulatory
system itself. This causes an even greater decrease in
cardiac output, and a vicious circle ensues, with
progressively increasing circulatory shock, less
adequate tissue perfusion, more shock, and so forth
until death. It is with this late stage of circulatory shock
that we are especially concerned, because appropriate
physiologic treatment can often reverse the rapid slide
to death.

Physiology of Cardiovascular shock.

Stages of Shock
• Because the characteristics of circulatory shock change
with different degrees of severity, shock is divided into the
following three major stages:
• A nonprogressive stage (sometimes called the
compensated stage), in which the normal circulatory
compensatory mechanisms eventually cause full recovery
without help from outside therapy.
• A progressive stage, in which, without therapy, the shock
becomes steadily worse until death.
• An irreversible stage, in which the shock has progressed to
such an extent that all forms of known therapy are
inadequate to save the person's life, even though, for the
moment, the person is still alive

Cardiovascular shock classification
• The causes are divided into four groups:
1. inadequate volume of blood to fill the vascular system
(hypovolemic shock);
2. increased size of the vascular system produced by
vasodilatation in the presence of a normal blood
volume (distributive, vasogenic, or low-resistance
shock);
3. inadequate output of the heart as a result of
myocardial abnormalities (cardiogenic shock);
4. inadequate cardiac output as a result of obstruction
of blood flow in the lungs or heart (obstructive
shock).

• Hypovolemic shock (decreased blood
volume) Hemorrhage Trauma Surgery Burns Fluid
loss associated with vomiting or diarrhea
• Distributive shock (marked vasodilation; also called
vasogenic or low-resistance shock) Fainting
(neurogenic shock) Anaphylaxis Sepsis (also causes
hypovolemia due to increased capillary permeability
with loss of fluid into tissues) Cardiogenic shock
(inadequate output by a diseased heart) Myocardial
infarction Congestive heart failure Arrhythmias
• Obstructive shock (obstruction of blood
flow) Tension pneumothorax Pulmonary
embolism Cardiac tumor Pericardial tamponade

DIAGNOSIS
• Recognizing the cause of shock is more important than categorizing the
type.
• Often, the cause is obvious or can be recognized quickly based on the
history and physical examination, aided by simple testing.
• Specific diagnosis criteria include obtundation, heart rate > 100,
respiratory rate > 22, hypotension (systolic BP < 90 mm Hg) or a 30-mm Hg
fall in baseline BP, and urine output < 0.5 mL/kg/h. Laboratory findings
that support the diagnosis include lactate > 3 mmol/L, base deficit < −4
mEq/L, and Paco2< 32 mm Hg. However, none of these findings alone is
diagnostic, and each is evaluated by its trend (ie, worsening or improving)
and in the overall clinical context, including physical signs.

Hypovolemic shock
• characterized by hypotension; a rapid, thready
pulse; cold, pale, clammy skin; intense thirst;
rapid respiration; and restlessness or,
alternatively, torpor. Urine volume is markedly
decreased. Hypovolemic shock is commonly
subdivided into categories on the basis of
cause. The use of terms such as hemorrhagic
shock, traumatic shock, surgical shock, and
burn shock

• In hypovolemic and other forms of shock,
inadequate perfusion of the tissues leads to
increased anaerobic glycolysis, with production of
large amounts of lactic acid. In severe cases, the
blood lactate level rises from a normal value of
about 1 mmol/L to 9 mmol/L or more. The
resulting lactic acidosis depresses the
myocardium, decreases peripheral vascular
responsiveness to catecholamines, and may be
severe enough to cause coma.

Compensatory Reactions Activated by
Hypovolemia.
• Vasoconstriction
• Tachycardia
• Venoconstriction
• Tachypnea Increased thoracic pumping
• Restlessness Increased skeletal muscle pumping (in some
cases)
• Increased movement of interstitial fluid into capillaries
• Increased secretion of vasopressin
• Increased secretion of glucocorticoids
• Increased secretion of renin and aldosterone
• Increased secretion of erythropoietin
• Increased plasma protein synthesis

Hypovolemic Shock Caused by Body Fluid Loss
Site of Fluid Loss Mechanism of Loss
Skin Thermal or chemical burn, sweating due to
excessive heat exposure
GI tract Vomiting, diarrhea
Kidneys Diabetes mellitus or insipidus, adrenal
insufficiency, salt-losing nephritis, the
polyuric phase after acute tubular
damage, use of potent diuretics
Intravascular fluid lost to the extravascular
space
Increased capillary permeability secondary
to inflammation or traumatic injury (eg,
crush), anoxia, cardiac arrest, sepsis, bowel
ischemia, acute pancreatitis

20
sympathetic
innervation of
myocardium
sympathetic innervation of
arterioles
Baroreceptors on aorta and carotid
sinus send information about
changes in BP to cardiovascular
centre
cardiovascular centre
sympathetic and
parasympathetic innervation
of Sino-atrial node
Control of Blood Pressure via the Baroreceptor Reflex
brain
key
parasympathetic nerves
sympathetic nerves
afferent sensory nerves
arterioles
heart
© Roger McFadden – University of Central England 2003

21
Renin – Angiotensin – Aldosterone Pathway
THIRST
ANGIOTENSIN II
ADRENAL
CORTEX
KIDNEYS increase Na+
reabsorption from filtrate
BP
VASOCONSTRICTION
BLOOD
PRESSURE
ALDOSTERONE
BLOOD
VOLUME
ANGIOTENSIN CONVERTING
ENZYME
JUXTAGLOMERULAR cells in the
kidney respond to a REDUCTION
IN BLOOD VOLUME from
EXCESS VOMITING, SWEATING,
& HAEMORRHAGE etc.
RENIN released into
blood
ANGIOTENSINOGEN ANGIOTENSIN I

22
osmoreceptors in hypothalamus detect
increase in osmolarity of blood
and release ADH
into blood stream
ADH
FILTRATE
ADH
water
urine blood
nephron capillary
ADH increases the
amount of water
reabsorbed from the
filtrate to the blood
urine output is reduced as more water is returned to
the blood
Role of ADH in dehydration

• decrease in pulse pressure or mean arterial pressure
decreases the number of impulses ascending to the
brain from the arterial baroreceptors, resulting in
increased vasomotor discharge. The resulting
vasoconstriction is generalized, sparing only the vessels
of the brain and the heart. The coronary vessels are
dilated because of the increased myocardial
metabolism secondary to an increase in heart rate.
Vasoconstriction in the skin accounts for the coolness
and pallor, and vasoconstriction in the kidneys
accounts for the shutdown in renal function.

• The immediate cardiac response to
hypovolemia is tachycardia. With more
extensive loss of volume tachycardia can be
replaced by bradycardia, whereas with very
severe hypovolemia tachycardia reappears.
Bradycardia may be due to unmasking of a
vagally mediated depressor reflex, perhaps
related to limiting blood loss.

• Vasoconstriction in the kidney reduces
glomerular filtration. This reduces water loss,
but it reaches a point at which nitrogenous
products of metabolism accumulate in the
blood (prerenal azotemia). If hypotension is
prolonged, there may be severe renal tubular
damage, leading to acute renal failure.

• The fall in blood pressure and the decreased O2-
carrying power of the blood caused by the loss of red
cells results in stimulation of the carotid and aortic
chemoreceptors. This not only stimulates respiration
but increases vasoconstrictor discharge. In severe
hypovolemia, the pressure is so low that there is no
longer any discharge from the carotid and aortic
baroreceptors. This occurs when the mean blood
pressure is about 70 mm Hg. Under these
circumstances, if the afferent discharge from the
chemoreceptors via the carotid sinus and vagus nerves
is stopped, there is a paradoxic further fall in blood
pressure rather than a rise.

• Hypovolemia causes a marked increase in the
circulating levels of the pressor hormones
angiotensin II, epinephrine, norepinephrine,
and vasopressin. ACTH secretion is also
increased, and angiotensin II and ACTH both
cause an acute increase in aldosterone
secretion. The resulting retention of Na+ and
water helps re-expand blood volume.

• Forms of Hypovolemic Shock
• Hemorrhagic shock is probably the most carefully studied
form of shock because it is easily produced in experimental
animals. With moderate hemorrhage (5–15 mL/kg body
weight), pulse pressure is reduced but mean arterial
pressure may remain normal. With more severe
hemorrhage, blood pressure always falls.
• After hemorrhage, the plasma protein lost in shed blood is
gradually replaced by hepatic synthesis, and the
concentration of plasma proteins returns to normal in 3–4
days. The increase in circulating erythropoietin increases
red blood cell formation, but it takes 4–8 weeks to restore
red cell counts to normal.

Sympathetic Reflex Compensations in
Shock-Their Special Value to Maintain
Arterial Pressure
• The decrease in arterial pressure after
hemorrhage, as well as decreases in pressures
in the pulmonary arteries and veins in the
thorax, causes powerful sympathetic reflexes
(initiated mainly by the arterial baroreceptors
and other vascular stretch receptors.

• These reflexes stimulate the sympathetic
vasoconstrictor system in most tissues of the
body, resulting in three important effects:
• (1) The arterioles constrict in most parts of the
systemic circulation, thereby increasing the
total peripheral resistance.
• (2) The veins and venous reservoirs constrict,
thereby helping to maintain adequate venous
return despite diminished blood volume.

• (3) Heart activity increases markedly,
sometimes increasing the heart rate from the
normal value of 72 beats/min to as high as
160 to 180 beats/min.

Protection of Coronary and Cerebral
Blood Flow by the Reflexes
• A special value of the maintenance of normal
arterial pressure even in the presence of
decreasing cardiac output is protection of
blood flow through the coronary and cerebral
circulatory systems. The sympathetic
stimulation does not cause significant
constriction of either the cerebral or the
cardiac vessels.

• In addition, in both vascular beds, local blood
flow auto regulation is excellent, which prevents
moderate decreases in arterial pressure from
significantly decreasing their blood flows.
Therefore, blood flow through the heart and
brain is maintained essentially at normal levels as
long as the arterial pressure does not fall below
about 70 mm Hg, despite the fact that blood flow
in some other areas of the body might be
decreased to as little as one third to one quarter
normal by this time because of vasoconstriction.

The factors that cause a person to
recover from moderate degree of
shock
• are all the negative feedback control mechanisms
of the circulation that attempt to return cardiac
output and arterial pressure back to normal
levels. They include the following:
1. Baroreceptor reflexes, which elicit powerful
sympathetic stimulation of the circulation.
2. Central nervous system ischemic response,
which elicits even more powerful sympathetic
stimulation throughout the body but is not
activated significantly until the arterial pressure
falls below 50 mm Hg.

3. Reverse stress-relaxation of the circulatory
system, which causes the blood vessels to
contract around the diminished blood volume so
that the blood volume that is available more
adequately fills the circulation.
4. Increased secretion of renin by the kidneys and
formation of angiotensin II, which constricts the
peripheral arteries and also causes decreased
output of water and salt by the kidneys, both of
which help prevent progression of shock.

5. Increased secretion by the posterior pituitary
gland of vasopressin (antidiuretic hormone),
which constricts the peripheral arteries and
veins and greatly increases water retention by
the kidneys.
6. Increased secretion by the adrenal medulla of
epinephrine and norepinephrine, which
constricts the peripheral arteries and veins
and increases the heart rate.

7. Compensatory mechanisms that return the
blood volume back toward normal, including
absorption of large quantities of fluid from the
intestinal tract, absorption of fluid into the
blood capillaries from the interstitial spaces of
the body, conservation of water and salt by
the kidneys, and increased thirst and
increased appetite for salt, which make the
person drink water and eat salty foods if able.

Progressive Shock/Vicious Circle and
Cardiovascular Deterioration
• Cardiac Depression; When the arterial
pressure falls low enough, coronary blood flow
decreases below that required for adequate
nutrition of the myocardium. This weakens the
heart muscle and thereby decreases the
cardiac output more. Thus, a positive
feedback cycle has developed, whereby the
shock becomes more and more severe.

• Vasomotor Failure -brain's vasomotor center
depresses so much that it, too, becomes progressively
less active and finally totally inactive. For instance,
complete circulatory arrest to the brain causes, during
the first 4 to 8 minutes, the most intense of all
sympathetic discharges, but by the end of 10 to 15
minutes, the vasomotor center becomes so depressed
that no further evidence of sympathetic discharge can
be demonstrated. Fortunately, the vasomotor center
usually does not fail in the early stages of shock if the
arterial pressure remains above 30 mm Hg.

• Blockage of Very Small Vessels-"Sludged
Blood." In time, blockage occurs in many of
the very small blood vessels in the circulatory
system and this also causes the shock to
progress

• Increased Capillary Permeability After many
hours of capillary hypoxia and lack of other
nutrients, the permeability of the capillaries
gradually increases, and large quantities of
fluid begin to transude into the tissues

• Release of Toxins by Ischemic Tissue shock
causes tissues to release toxic substances,
such as histamine, serotonin, and tissue
enzymes

• Traumatic shock develops when there is severe
damage to muscle and bone. This is the type of
shock seen in battle casualties and automobile
accident victims. Bleeding into the injured areas
is the principal cause of such shock. The amount
of blood that can be lost into a site of injury that
appears relatively minor is remarkable; the thigh
muscles can accommodate 1 L of extravasated
blood, for example, with an increase in the
diameter of the thigh of only 1 cm.

• Breakdown of skeletal muscle is a serious additional
problem when shock is accompanied by extensive
crushing of muscle (crush syndrome). When pressure
on tissues is relieved and they are once again perfused
with blood, free radicals are generated, which cause
further tissue destruction (reperfusion-induced
injury). Increased Ca2+ in damaged cells can reach toxic
levels. Large amounts of K+ enter the circulation.
Myoglobin and other products from reperfused tissue
can accumulate in kidneys in which glomerular
filtration is already reduced by hypotension, and the
tubules can become clogged, causing anuria.

• Surgical shock is due to combinations, in various
proportions, of external hemorrhage, bleeding
into injured tissues, and dehydration.
• In burn shock, there is loss of plasma from burn
surfaces and the hematocrit rises rather than
falls, producing severe hemoconcentration. There
are, in addition, complex metabolic changes. For
these reasons, plus the problems of easy
infection of burned areas and kidney damage, the
mortality rate when third-degree burns cover
more than 75% of the body is close to 100%.

Distributive Shock
• In distributive shock, most of the symptoms and
signs described previously are present. However,
vasodilation causes the skin to be warm rather
than cold and clammy.
• Anaphylactic shock is a good example of
distributive shock. In this condition, an
accelerated allergic reaction causes release of
large amounts of histamine, producing marked
vasodilation. Blood pressure falls because the size
of the vascular system exceeds the amount of
blood in it even though blood volume is normal.

• neurogenic shock, a sudden burst of
autonomic activity results in vasodilation and
pooling of blood in the veins. The resulting
decrease in venous return reduces cardiac
output and frequently produces fainting, or
syncope, a sudden transient loss of
consciousness. A common form is postural
syncope, which occurs on rising from a sitting
or lying position.

• This is common in patients taking drugs that
block sympathetic discharge or its effects on
the blood vessels. Falling to the horizontal
position restores blood flow to the brain, and
consciousness is regained. Pressure on the
carotid sinus produced, for example, by a tight
collar can cause sufficient bradycardia and
hypotension to cause fainting (carotid sinus
syncope).

• Fainting brought on by a variety of activities
has been given appropriate names such as
micturition syncope, cough syncope,
deglutition syncope, and effort syncope

septic shock
• This is the most common cause of death in
ICUs. It is a complex condition that includes
elements of hypovolemic shock resulting from
loss of plasma into the tissues ("third
spacing") and cardiogenic shock resulting from
toxins that depress the myocardium. It is
associated with excess production of NO, and
therapy with drugs that scavenge NO may be
beneficial.

• The hallmark of septic shock is a decrease in
peripheral vascular resistance that occurs
despite increased levels of vasopressor
catecholamines. Before this vasodilatory
phase, many patients experience a period
during which oxygen delivery to tissues is
compromised by myocardial depression,
hypovolemia, and other factors.

• During this "hypodynamic" period, the blood
lactate concentration is elevated, and central
venous oxygen saturation is low. Fluid
administration is usually followed by the
hyperdynamic, vasodilatory phase during
which cardiac output is normal (or even high)
and oxygen consumption is independent of
oxygen delivery.

• The blood lactate level may be normal or
increased, and normalization of the central
venous oxygen saturation (SvO2) may reflect
either improved oxygen delivery or left-to-
right shunting.

VASODILATORS
• Prominent hypotensive
molecules include nitric oxide,
-endorphin, bradykinin, PAF,
and prostacyclin.

• However, in clinical trials, neither a PAF
receptor antagonist nor a bradykinin
antagonist improved survival rates among
patients with septic shock, and a nitric oxide
synthetase inhibitor, L-NG-methylarginine HCl,
actually increased the mortality rate.

Severe Sepsis: A Single Pathogenesis?
• In some cases, circulating bacteria and their
products almost certainly elicit multiorgan
dysfunction and hypotension by directly
stimulating inflammatory responses within
the vasculature. In patients with fulminant
meningococcemia, for example, mortality
rates have correlated well with blood
endotoxin levels and with the occurrence of
DIC.

• In most patients with nosocomial infections, in
contrast, circulating bacteria or bacterial
molecules may reflect uncontrolled infection
at a local tissue site and have little or no direct
impact on distant organs; in these patients,
inflammatory mediators or neural signals
arising from the local site seem to be the key
triggers for severe sepsis and septic shock

SITE OF SEPSIS Vs SEVERITY
• In a large series of patients with positive blood
cultures, the risk of developing severe sepsis was
strongly related to the site of primary infection:
bacteremia arising from a pulmonary or
abdominal source was eightfold more likely to be
associated with severe sepsis than was
bacteremic urinary tract infection, even after the
investigators controlled for age, the kind of
bacteria isolated from the blood, and other
factors.

• Some of the typical causes of septic shock
include the following:
• Peritonitis caused by spread of infection from
the uterus and fallopian tubes, sometimes
resulting from instrumental abortion
performed under unsterile conditions.
• Peritonitis resulting from rupture of the
gastrointestinal system, sometimes caused by
intestinal disease and sometimes by wounds.

• Generalized bodily infection resulting from
spread of a skin infection such as streptococcal or
staphylococcal infection.
• Generalized gangrenous infection resulting
specifically from gas gangrene bacilli, spreading
first through peripheral tissues and finally by way
of the blood to the internal organs, especially the
liver.
• Infection spreading into the blood from the
kidney or urinary tract, often caused by colon
bacilli.

• A third pathogenesis may be represented by
severe sepsis due to superantigen-producing
Staphylococcus aureus or Streptococcus
pyogenes, since the T cell activation induced
by these toxins produces a cytokine profile
that differs substantially from that elicited by
gram-negative bacterial infection.

• In summary, the pathogenesis of severe sepsis
may differ according to the infecting microbe,
the ability of the host's innate defense
mechanisms to sense it, the site of the
primary infection, the presence or absence of
immune defects, and the prior physiologic
status of the host

• Genetic factors may also be important. For
example, studies in different ethnic groups
have identified associations between allelic
polymorphisms in TLR4, caspase 12L, TNF-,
and IFN- genes and the risk of developing
severe sepsis.

Cardiogenic Shock
• When the pumping function of the heart is
impaired to the point that blood flow to
tissues is no longer adequate to meet resting
metabolic demands, cardiogenic shock
results. This is most commonly due to
extensive infarction of the left ventricle but
can also be caused by other diseases that
severely compromise ventricular function.

• The symptoms are those of hypovolemic
shock plus congestion of the lungs and viscera
resulting from failure of the heart to put out
all the venous blood returned to it.
Consequently, the condition is sometimes
called "congested shock." The incidence of
shock in patients with myocardial infarction is
about 10%, and the mortality rate is 60–90%.

• 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]. It is associated
with in-hospital mortality rates >50%.

CAUSES
• Circulatory failure based on cardiac
dysfunction may be caused by primary
myocardial failure, most commonly secondary
to acute myocardial infarction (MI), and less
frequently by cardiomyopathy or myocarditis
or cardiac tamponade.

• *Intrinsic causes:
• Hearth muscle damage
• Acute MI
• CHF
• Obstructive
• Dysrhthmia
• Valvular distruption
• *Extrinsic causes(cause obstructive shock):
• Cardiac Tamponade
• Tension Pneumothorax
• *Symptoms and Signs
• Cool, clammy, pale, cyanotic skin, BP drop, capillary refill.

Mechanisms of Cardiogenic and Obstructive Shock
Type Mechanism Cause
Obstructive Mechanical interference
with ventricular filling
Tension pneumothorax,
cava compression, cardiac
tamponade, atrial tumor
or clot
Interference with
ventricular emptying
Pulmonary embolism
Cardiogenic Impaired myocardial
contractility
Myocardial ischemia or
MI, myocarditis, drugs
Abnormalities of cardiac
rhythm
Tachycardia, bradycardia
Cardiac structural
disorder
Acute mitral or aortic
regurgitation, ruptured
interventricular septum,
prosthetic valve
malfunction

• Etiologies of Cardiogenic Shock or Pulmonary Edema
• Acute myocardial infarction/ischemia
• LV failure
• VSR
• Papillary muscle/chordal rupture—severe MR
• Ventricular free wall rupture with subacute
tamponade
• Other conditions complicating large MIs
• Hemorrhage
• Infection
•

• Excess negative inotropic or vasodilator
medications
• Prior valvular heart disease
• Hyperglycemia/ketoacidosis
• Post-cardiac arrest
• Post-cardiotomy
• Refractory sustained tachyarrhythmias
• Acute fulminant myocarditis
• End-stage cardiomyopathy

• Left ventricular apical ballooning
• Takotsubo cardiomyopathy
• Hypertrophic cardiomyopathy with severe outflow
obstruction
• Aortic dissection with aortic insufficiency or tamponade
• Pulmonary embolus
• Severe valvular heart disease
• Critical aortic or mitral stenosis
• Acute severe aortic or MR
• Toxic-metabolic
• Beta-blocker or calcium channel antagonist overdose

• Other Etiologies of Cardiogenic Shock
• RV failure due to:
• Acute myocardial infarction
• Acute co-pulmonale
• Refractory sustained bradyarrhythmias
• Pericardial tamponade
• Toxic/metabolic
• Severe acidosis, severe hypoxemia

Pathophysiology of cardiogenic shock.
• CS is characterized by a vicious circle in which
depression of myocardial contractility, usually
due to ischemia, results in reduced cardiac
output and arterial pressure (BP), which result in
hypoperfusion of the myocardium and further
ischemia and depression of the cardiac output.
Systolic myocardial dysfunction reduces stroke
volume and, together with diastolic dysfunction,
leads to elevated LV end-diastolic pressure and
PCWP as well as to pulmonary congestion.

• Reduced coronary perfusion leads to worsening
ischemia and progressive myocardial dysfunction
and a rapid downward spiral, which, if
uninterrupted, is often fatal. A systemic
inflammatory response syndrome may
accompany large infarctions and shock.
Inflammatory cytokines, inducible nitric oxide
synthase, and excess nitric oxide and
peroxynitrite may contribute to the genesis of CS
as they do to other forms of shock.

• Lactic acidosis from poor tissue perfusion and
hypoxemia from pulmonary edema may result
from pump failure and then contribute to the
vicious circle by worsening myocardial
ischemia and hypotension. Severe acidosis (pH
< 7.25) reduces the efficacy of endogenous
and exogenously administered
catecholamines. Refractory sustained
ventricular or atrial tachyarrhythmias can
cause or exacerbate CS.

• Autopsy specimens often reflect the stuttering
course and piecemeal necrosis of the LV,
showing varying stages of infarction.
Reinfarction is apparent as new areas of
necrosis contiguous with or remote from a
slightly older infarct. Infarctions that extend
through the full myocardial thickness and
result in rupture of the interventricular
septum, papillary muscle, or ventricular free
wall may result in shock.

Obstructive Shock(extracardiac)
• The picture of congested shock is also seen in
obstructive shock. Causes include massive
pulmonary emboli, tension pneumothorax
with kinking of the great veins, and bleeding
into the pericardium with external pressure on
the heart (cardiac tamponade).

• In the latter two conditions, prompt surgery is
required to prevent death. Pulsus paradoxus
occurs in cardiac tamponade. Normally, blood
pressure falls about 5 mm Hg during
inspiration.

• In pulsus paradoxus, this response is
exaggerated, and blood pressure falls 10 mm
Hg or more as a result of increased pressure of
the fluid in the pericardial sac on the external
surface of the heart. However, pulsus
paradoxus also occurs with labored respiration
in severe asthma, emphysema, and upper
airway obstruction.

Treatment:
* Aims
- Correct the cause
- Assist compensatory mechanism to restore an
adequate level of tissue perfusion
* Volume resuscitation
- Enternal route
* Intervenous route
85

• Cardiogenic shock is an emergency requiring
immediate resuscitative therapy before shock
irreversibly damages vital organs. The key to a
good outcome in patients with cardiogenic
shock is an organized approach, with rapid
diagnosis and prompt initiation of
pharmacologic therapy to maintain blood
pressure and cardiac output.

• PROCEDURES:
• Central venous line placement- ressussitation,
monitoring
• Pulmonary artery catheter
• Intraaortic baloon pump
• Pci and CARBG- PCI or coronary artery bypass is the
treatment of choice for cardiogenic shock and that
each has been shown to markedly decrease mortality
rates at 1 year. PCI should be initiated within 90
minutes of presentation; however, it remains helpful,
as an acute intervention, within 12 hours of
presentation.

• Thrombolytics
• Consultation with a cardiologist.
• echocardiographic support, placement of an
intra-aortic balloon pump (IABP), and transfer
to more definitive care (eg, cardiac
catheterization suite, ICU, operating room). In
severe cases, also consider discussing the case
with a cardiothoracic surgeon.

• Pharmacotherapy
• Ionotropics augment coronary and cerebral blood
flow (dopamine,bobutamine,norepinephrinemilrinone,
inamrinone)
• Vasodilators decrease preload and afterload-
nitroglyceride- This agent causes relaxation of vascular
smooth muscle by stimulating intracellular cyclic
guanosine monophosphate production
• Antiplatelets
• Analgesia-opiods decrease sympathetic stress and
provide preload reduction.

90
Irreversible Shock (complication) leads to:
• Renal failure
• Hepatic failure
• Multiple organ systems failure
• Adult respiratory distress syndrome
• Death

EFFECTS ON CO,PCWP AND SVR
Etiology CO PCWP SVR
cardiogenic decreased increased increased
hypovolemic decreased decreased increased
distributive increased decreased decreased
obstructive decreased Increased increased

REFERENCES
• Guyton and hall textbook of medical
physiology
• Medical Physiology-Ganong
• Emedicine -
http://emedicine.medscape.com/article/1521
91-overview
• Harrison internal medicine
• Merck Manuals

Physiology of Cardiovascular shock.

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