Lec 6 ‫ احمد فاضل ابراهيم‬.‫د‬.‫م‬.

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Shock
SHOCK
Shock is a systemic state of low tissue perfusion which is inadequate for normal
cellular respiration. With insufficient delivery of oxygen and glucose, cells switch
from aerobic to anaerobic metabolism. If perfusion is not restored in a timely
fashion, cell death ensues.

Pathophysiology
Cellular
As perfusion to the tissues is reduced, cells are deprived of oxygen and must switch
from aerobic to anaerobic metabolism.
The product of anaerobic respiration is lactic acid. When enough tissue is under-
perfused, the accumulation of lactic acid in the blood produces a systemic metabolic
acidosis.
As glucose within cells is exhausted, anaerobic respiration ceases and there is failure
of sodium/potassium pumps in the cell membrane and intracellular organelles.
Intracellular lysosomes release autodigestive enzymes and cell lysis ensues.
Intracellular contents, including potassium are released into the blood stream.
Microvascular
As tissue ischemia progresses, these changes result in activation of the immune and
coagulation systems. Hypoxia and acidosis activate complement and prime
neutrophils, resulting in the generation of oxygen free radicals and cytokine release.
These mechanisms lead to injury of the capillary endothelial cells. These, in turn,
further activate the immune and coagulation systems. Damaged endothelium loses
its integrity and becomes ‘leaky’. Spaces between endothelial cells allow fluid to
leak out and tissue oedema ensues, exacerbating cellular hypoxia.
Systemic
Cardiovascular
As preload and afterload decrease, there is a compensatory baroreceptor response
resulting in increased sympathetic activity and release of catecholamines into the
circulation. This results in tachycardia and systemic vasoconstriction (except in
sepsis)
Respiratory
The metabolic acidosis and increased sympathetic response result in an increased
respiratory rate and minute ventilation to increase the excretion of carbon dioxide
(and so produce a compensatory respiratory alkalosis).
Renal
Decreased perfusion pressure in the kidney leads to reduced filtration at the
glomerulus and a decreased urine output. The renin–angiotensin–aldosterone axis is
stimulated, resulting in further vasoconstriction and increased sodium and water
reabsorption by the kidney.
Endocrine
As well as activation of the adrenal and renin–angiotensin systems, vasopressin
(antidiuretic hormone) is released from the hypothalamus in response to decreased
preload and results in vasoconstriction and resorption of water in the renal collecting
system. Cortisol is also released from the adrenal cortex contributing to the sodium
and water resorption and sensitizing the cells to catecholamines.

Ischemia–reperfusion syndrome
During the period of systemic hypoperfusion, cellular and organ damage progresses
due to the direct effects of tissue hypoxia and local activation of inflammation.
Further injury occurs once normal circulation is restored to these tissues. The acid
and potassium load that has built up can lead to direct myocardial depression,
vascular dilatation and further hypotension. The cellular and humoral elements
activated by the hypoxia (complement, neutrophils, microvascular thrombi) are
flushed back into the circulation where they cause further endothelial injury to
organs such as the lungs and the kidneys.
This leads to acute lung injury, acute renal injury, multiple organ failure and death.
Reperfusion injury can currently only be attenuated by reducing the extent and
duration of tissue hypoperfusion.
Classification of shock
All types of shock are characterized by systemic tissue hypoperfusion and different
states may coexist within the same patient.
Hypovolemic shock
Hypovolemic shock is due to a reduced circulating volume. Hypovolemia may be
due to hemorrhagic or non-hemorrhagic causes. Non-hemorrhagic causes include
poor fluid intake (dehydration), excessive fluid loss due to vomiting, diarrhea,
urinary loss (e.g. diabetes), evaporation, or ‘third-spacing’ where fluid is lost into
the gastrointestinal tract and interstitial spaces, as for example in bowel obstruction
or pancreatitis.
Hypovolemia is probably the most common form of shock, and to some degree is a
component of all other forms of shock. Absolute or relative hypovolemia must be
excluded or treated in the management of the shocked state, regardless of cause.

Cardiogenic shock
Cardiogenic shock is due to primary failure of the heart to pump blood to the tissues.
Causes of cardiogenic shock include myocardial infarction, cardiac dysrhythmias,
valvular heart disease, blunt myocardial injury and cardiomyopathy. Cardiac
insufficiency may also be due to myocardial depression due to endogenous factors
(e.g. bacterial and humoral agents released in sepsis) or exogenous factors, such as
pharmaceutical agents or drug abuse. Evidence of venous hypertension with
pulmonary or systemic oedema may coexist with the classical signs of shock.
Obstructive shock
In obstructive shock there is a reduction in preload due to mechanical obstruction of
cardiac filling. Common causes of obstructive shock include cardiac tamponade,
tension pneumothorax, massive pulmonary embolus or air embolus. In each case,
there is reduced filling of the left and/or right sides of the heart leading to reduced
preload and a fall in cardiac output.
Distributive shock
Distributive shock describes the pattern of cardiovascular responses characterizing
a variety of conditions, including septic shock, anaphylaxis and spinal cord injury.
Inadequate organ perfusion is accompanied by vascular dilatation with hypotension,
low systemic vascular resistance, inadequate afterload and a resulting abnormally
high cardiac output.
In anaphylaxis, vasodilatation is due to histamine release, while in high spinal cord
injury there is failure of sympathetic outflow and adequate vascular tone (neurogenic
shock). The cause in sepsis is less clear but is related to the release of bacterial
products (endotoxin) and the activation of cellular and humoral components of the
immune system. There is maldistribution of blood flow at a microvascular level with
arteriovenous shunting and dysfunction of cellular utilization of oxygen.
Endocrine shock
Endocrine shock may present as a combination of hypovolemic, cardiogenic or
distributive shock. Causes of endocrine shock include hypo- and hyperthyroidism
and adrenal insufficiency.
Hypothyroidism causes a shock state similar to that of neuro genic shock due to
disordered vascular and cardiac responsiveness to circulating catecholamines.
Cardiac output falls due to bradycardia & cardiomyopathy.
Thyrotoxicosis may cause a high-output cardiac failure.
Adrenal insufficiency leads to shock due to hypovolemia and a poor response to
circulating and exogenous catecholamines.
Adrenal insufficiency may be due to pre-existing Addison’s disease or be a relative
insufficiency due to a pathological disease state, such as systemic sepsis.

Consequences

Un-resuscitatable shock
Patients who are in profound shock for a prolonged period of time become ‘un-
resuscitatable’. Cell death follows from cellular ischemia and the ability of the body
to compensate is lost.
There is myocardial depression and loss of responsiveness to fluid or inotropic
therapy. Peripherally there is loss of the ability to maintain systemic vascular
resistance and further hypotension ensues. The peripheries no longer respond
appropriately to vasopressor agents. Death is the inevitable result.
This stage of shock is the combined result of the severity of the insult and delayed,
inadequate or inappropriate resuscitation in the earlier stages of shock.

Multiple organ failure

As techniques of resuscitation have improved, more and more patients are surviving
shock. Where intervention is timely and the period of shock is limited, patients may
make a rapid, uncomplicated recovery. However, the result of prolonged systemic
ischemia and reperfusion injury is end-organ damage and multiple organ failure.
Multiple organ failure is defined as two or more failed organ system
Management is supporting of organ systems with ventilation, cardiovascular support
and hemofiltration/dialysis until there is recovery of organ function. Multiple organ
failure currently carries a mortality of 60 per cent; thus, prevention is vital by early
aggressive identification and reversal of shock.
 RESUSCITATION

Once ‘airway’ and ‘breathing’ are assessed and controlled, attention is directed to
cardiovascular resuscitation.
Conduct of resuscitation
1- Resuscitation should not be delayed in order to definitively diagnose the
source of the shocked state. However, the timing and nature of resuscitation
will depend on the type of shock and the timing and severity of the insult.
If there is initial doubt about the cause of shock, it is safer to assume the cause
is hypovolemia and begin with fluid resuscitation, and then assess the
response.
2- In patients who are actively bleeding (major trauma, aortic aneurysm rupture,
gastrointestinal hemorrhage), it is counterproductive to institute high-volume
fluid therapy without controlling the site of hemorrhage. Increasing blood
pressure merely increases bleeding from the site while fluid therapy cools the
patient and dilutes available coagulation factors. Thus, operative hemorrhage
control should not be delayed and resuscitation should proceed in parallel with
surgery.
3- Conversely, a patient with bowel obstruction and hypovolemic shock must be
adequately resuscitated before undergoing surgery otherwise the additional
surgical injury and hypovolemia induced during the procedure will exacerbate
the inflammatory activation and increase the incidence and severity of end-
organ insult.

Fluid therapy
In all cases of shock, regardless of classification, hypovolemia and inadequate
preload must be addressed before other therapy is instituted. Administration of
inotropic or chronotropic agents to an empty heart will rapidly and permanently
deplete the myocardium of oxygen stores and dramatically reduce diastolic filling
and therefore coronary perfusion. Patients will enter the un-resuscitatable stage of
shock as the myocardium becomes progressively more ischemic and unresponsive
to resuscitative attempts.
First-line therapy, therefore, is intravenous access and administration of intravenous
fluids. Access should be through short, wide-bore catheters that allow rapid infusion
of fluids
as necessary. Long, narrow lines, such as central venous catheters, have too high a
resistance to allow rapid infusion and are more appropriate for monitoring than fluid
replacement therapy.
Type of fluids
There is continuing debate over which resuscitation fluid is best for the management
of shock. There is no ideal resuscitation fluid, and it is more important to understand
how and when to administer it. In most studies of shock resuscitation there is no
overt difference in response or outcome between crystalloid solutions (normal
saline, Hartmann’s solution, Ringer’s lactate) or colloids (albumin or commercially
available products).

Monitoring for patients in shock

Minimum
- ECG
-Pulse oximetry
-Blood pressure
-Urine output
Additional modalities
- Central venous pressure (Invasive blood pressure)
- Cardiac output
- Base deficit and serum lactate

Central venous pressure

There is no ‘normal’ central venous pressure (CVP) for a shocked patient, CVP
measurements should be assessed dynamically as response to a fluid challenge A
fluid bolus (250– 500 mL) is infused rapidly over 5–10 minutes.
The normal CVP response is a rise of 2–5 cmH2O which gradually drifts back to the
original level over 10–20 minutes. Patients with no change in their CVP are empty
and require further fluid resuscitation. Patients with a large, sustained rise in CVP
have high preload .
Cardiac output
Measurement of cardiac output, systemic vascular resistance and preload can help
distinguish the types of shock present (hypovolemia, distributive, cardiogenic),
especially when they coexist.
Measurement of cardiac output is desirable in patients who do not respond as
expected to first-line therapy, or who have evidence of cardiogenic shock or
myocardial dysfunction.

Base deficit and lactate

Lactic acid is generated by cells undergoing anaerobic respiration. The degree of
lactic acidosis, as measured by serum lactate level and/or the base deficit, is sensitive
for both diagnosis of shock and monitoring the response to therapy. Patients with a
base deficit over 6 mmol/L have a much higher morbidity and mortality than those
with no metabolic acidosis. Furthermore, the duration of time in shock with an
increased base deficit is important, even if all other vital signs have returned to
normal.

End points of resuscitation

Traditionally, patients have been resuscitated until they have a normal pulse, blood
pressure and urine output.
However, these parameters are monitoring organ systems whose blood flow is
preserved until the late stages of shock. A patient therefore may be resuscitated to
restore central perfusion to the brain, lungs and kidneys and yet continue to under
perfuse the gut and muscle beds. Thus, activation of inflammation and coagulation
may be ongoing and lead to reperfusion injury when these organs are finally
perfused, and ultimately multiple organ failure.
This state of normal vital signs and continued under-perfusion is termed ‘occult
hypoperfusion’. With current monitoring techniques, it is manifested only by a
persistent lactic acidosis and low mixed venous oxygen saturation. The duration
patients spend in this hypo-perfused state has a dramatic effect on outcome.
Patients with occult hypoperfusion for more than 12 hours have two to three times
the mortality of patients with a limited duration of shock.

-THE END-