physiology and mli of shock
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DEFINITION
SHOCK- A physiological state characterized by a
significant, systemic
reduction in tissue perfusion,
resulting in decreased tissue oxygen delivery and
insufficient removal of cellular metabolic products,
resulting in tissue injury.
Shock usually results from inadequate cardiac output.
Two types of factors can severely reduce cardiac
output
Cardiac abnormalities that decrease the ability of the
heart to pump blood
Factors that decrease the venous return which can
be due to
diminished blood volume
decreased vascular tone
obstruction to the blood flow
Classification of shock
Primary Shock: shock that has a neurogenic
basis in which pain and psychic factors affect
the vascular system.
Occurs immediately after an insult.
Secondary shock: shock that occurs sometime
after the injury (6 to 24 hours later).
It is associated with changes in capillary
permeability and subsequent loss of plasma into
the tissue spaces.
Based on etiology classified into
Hypovolemic Shock (decreased blood volume)
Includes- Hemorrhage, trauma, surgery, burns, fluid loss due to
vomiting or diarrhea
Cardiogenic Shock( inadequate output by the diseased heart)
Includes- myocardial infarction, congestive heart failure,
arrhythmias.
Obstructive Shock (obstruction to the blood flow)
Includes- tension pneumothorax, Pulmonary embolism, cardiac
tamponade
Distributive Shock (marked vasodilation, low resistant Shock)
Includes- anaphylaxis, sepsis, Neurogenic, metabolic, psychogenic
shock.
Stages of Shock:
shock tends to evolve through three phases:
An initial non-progressive phase or compensatory stage during
which reflex compensatory mechanisms are activated and
perfusion of vital organs is maintained
A progressive stage characterized by tissue hypo-perfusion and
onset of worsening circulatory and metabolic imbalances,
including acidosis
An irreversible stage that sets in after the body has incurred
cellular and tissue injury so severe that even if the hemodynamic
defects are corrected, survival is not possible
Pathophysiology of Shock
Regardless of etiology, the initial physiologic responses in shock
are driven by tissue hypoperfusion and the developing cellular
energy deficit.
The imbalance between cellular supply and demand leads to
neuroendocrine and inflammatory responses, the magnitude of
which is usually proportional to the degree and duration of shock.
The specific responses will differ based on the etiology of shock, as
certain physiologic responses may be limited by the inciting
pathology
The pathophysiologic responses also vary with time and in
response to resuscitation.
Specific responses in Shock
Neuroendocrine Response
Baroreceptors- elicits powerful sympathetic stimulation of
circulation, producing centrally mediated constriction of peripheral
vessels.
Chemoreceptors-Stimulation results in vasodilation of the coronary
arteries, slowing of the heart rate, and vasoconstriction of the
splanchnic and skeletal circulation.
The sensation of pain from injured tissue is transmitted via the
spinothalamic tracts, resulting in activation of the hypothalamic-
pituitary-adrenal axis, as well as activation of the ANS to induce
direct sympathetic stimulation of the adrenal medulla to release
catechol amines.
Cardiovascular response
Cardiac output, the major determinant of tissue
perfusion, is the product of stroke volume and
heart rate.
Hypovolemia leads to reduced Stroke volume
Tachycardia develops as compensation
Increased myocardial O2 consumption occurs as
a result of the increased workload
Ischemia and infarction worsens
Sepsis, severe tissue trauma, hypothermia, general anesthesia,
and acidemia may all also impair myocardial contractility and
reduce the stroke volume at any given ventricular end-diastolic
volume.
The resistance to ventricular ejection, influenced by the
systemic vascular resistance, is elevated in most forms of shock.
Active venoconstriction as a consequence of adrenergic
activity is an important compensatory mechanism for the
maintenance of venous return and therefore of ventricular filling
during shock.
Microcirculation
Homeostatic vasoconstriction occurs in response to shock
The arteriolar and precapillary sphincter control fails as a result of
hypoxia and the effect of vasodilating agents
The venular channels are less sensitive to hypoxia and resist to
some degree the dilating effect of local metabolites.
Capillary engorgement follows and flow is sluggish or stagnant
microthrombus formation, or the passage of small white
microemboli, can be seen in the postcapillary venules
Capillary dysfunction also occurs secondary to activation of
endothelial cells by circulating inflammatory mediators
generated in septic or traumatic shock
Hormonal Response
Shock stimulates the hypothalamus and pituitary to release ACTH cortisol from adrenal cortex induce a
catabolic state.
Cortisol stimulates gluconeogenesis and insulin resistance
Cortisol also causes retention of sodium and water by the
nephrons of the kidney.
The renin-angiotensin system is activated in shock
producing angiotensin II which is a potent vasoconstrictor
of both splanchnic and peripheral vascular beds.
The pituitary also releases vasopressin or ADH in response to
hypovolemia
Epinephrine, angiotensin II, pain, and hyperglycemia also
increase production of ADH.
ADH acts on the distal tubule and collecting duct of the nephron
to increase water permeability, decrease water and sodium
losses, and preserve intravascular volume
ADH acts as a potent mesenteric vasoconstrictor, shunting
circulating blood away from the splanchnic organs during
hypovolemia.
This may contribute to intestinal ischemia and predispose to
intestinal mucosal barrier dysfunction in shock states.
It also increases hepatic gluconeogenesis and increases hepatic
glycolysis.
Metabolic effects
Decreased Oxygen tension Decreased ATP
production Anerobic metabolism Metabolic
acidosis
Decreased intracellular pH also influences vital cellular
functions such as normal enzyme activity, cell
membrane ion exchange, and cellular metabolic
signaling
Furthermore, acidosis leads to changes in calcium
metabolism and calcium signaling. Compounded,
these changes may lead to irreversible cell injury and
death.
Hepatic glycogenolysis, gluconeogenesis, ketogenesis,
skeletal muscle protein breakdown, and adipose tissue
lipolysis are increased by catecholamines.
Epinephrine induces further release of glucagon, while
inhibiting the pancreatic -cell release of insulin leading
to hyperglycemia and insulin resistance during shock
and injury.
The relative underuse of glucose by peripheral tissues
preserves it for the glucose-dependent organs such as
the heart and brain.
Immune and Inflammatory Responses
Alterations in the activity of the innate host immune
system can be responsible for both the
Development of shock (i.e., septic shock following severe
infection and traumatic shock following tissue injury with
hemorrhage) and
Pathophysiologic sequel of shock such as the
proinflammatory changes seen following hypoperfusion.
The inflammatory and immune responses can arise in
response to trauma, infection, ischemia, toxic, or
autoimmune stimuli.
Following direct tissue injury or infection
There is release of bioactive peptides by neurons in
response to pain
there is release of intracellular molecules by broken
cells, such as heat shock proteins, mitochondrial
peptides, heparan sulfate, high mobility group box 1,
and RNA [damage associated molecular patterns
(DAMP) ]
release of intracellular products from damaged and
injured cells can effects on distant tissues to activate
the inflammatory and immune responses.
Monocytes, macrophages, and T cells release potent
proinflammatory cytokines like Tumor necrosis factor
alpha and interleukins.
TNF- can produce peripheral vasodilation,
activate the release of other cytokines,
induce procoagulant activity, and
stimulate a wide array of cellular metabolic
changes.
IL-1 produces a febrile response to injury by
activating prostaglandins and causes anorexia by
activating the satiety center.
increased IL-2 secretion promotes shock-induced
tissue injury and the development of shock.
IL-6 contributes to lung, liver, and gut injury after
hemorrhagic shock.
IL-6 may play a role in the development of diffuse
alveolar damage and ARDS.
Specific types of Shock
Hypovolumic shock
Loss of blood (hemorrhagic)
External bleeding (wound to the outside)
Internal bleeding (hematoma, hemothorax, hemopertitoneum)
Loss of plasma
Burns
Loss of fluids and electrolytes
External (vomiting, diarrhea, excessive sweating)
Internal ( “third spacing” = pancreatitis, ascitis, bowl obstruction
Mild (loss of < 20% blood volume)
Few external signs in supine young patients
Moderate (loss of 20-40% blood volume)
Patient becomes increasingly anxious and
tachycardic >100 beats/min (sympathetic response)
oliguria
blood pressure may be maintained in supine patient
Severe (loss of > 40% blood volume)
Classic signs of shock appear with hemodynamic
instability
Signs and Symptoms
Low Blood Pressure
Systolic BP is usually below 90 mmHg
Pulse is rapid and weak
Respiration is rapid and shallow
Skin is pale, cool, and clammy
Drowsiness
CARDIOGENIC SHOCK
Pump failure
Secondary to myocardial infarction (most common)
Cardio-myophathy
Acute valvular dysfunction (regurgitations)
Rupture of the ventricular septum
Arrhythmia
Tachyarrhythmia
Bradyarrhythmia
Characteristics of Cardiogenic Shock
Low cardiac output
Peripheral vasoconstriction
Left sided heart failure leads to pulmonary
venous congestion and pulmonary edema
Right sided heart failure leads to systemic
venous congestion and peripheral edema
Signs and symptoms
Major difference between other types of shock is
presence of Pulmonary Edema
Difficulty breathing
Wheezes, Crackles, Rales are heard as fluid levels
increase
Productive cough with white or pink-tinged foamy
sputum
Cyanosis
Altered mentation
Oliguria ( decreased urination)
Obstructive shock
Tension pneumothorax
•Air trapped in pleural space with 1 way valve, air/pressure builds up
•Mediastinum shifted impeding venous return
Cardiac tamponade
•Blood in pericardial sac prevents venous return to and contraction of heart
Pulmonary embolism and Aortic stenosis
Resistance to ejection causes decreased cardiac function
Anaphylactic Shock
A type of distributive shock that results from widespread systemic allergic reaction to an antigen
Antigen exposure
body stimulated to produce IgE antibodies specific to antigen
drugs, bites, contrast, blood, foods, vaccines
Reexposure to antigen
IgE binds to mast cells and basophils
Anaphylactic response
Anaphylactic response
Vasodilatation
Increased vascular permeability
Bronchoconstriction
Increased mucus production
Increased inflammatory mediators recruitment
to sites of antigen interaction
Signs and symptoms
Almost immediate response to inciting antigen
Cutaneous manifestations
urticaria, erythema, pruritis, angioedema
Respiratory compromise
stridor, wheezing, bronchorrhea, respiratory
distress
Circulatory collapse
tachycardia, vasodilation, hypotension
Septic shock
Sepsis is defined as a systemic inflammatory
response to a bacterial infection with bacteriemia
(though blood cultures can be negative)
Severe sepsis is defined by additional end-organ
dysfunction (mortality rate: 25-30%)
Septic shock is defined as sepsis with hypotension
despite fluid resuscitation and evidence of
inadequate tissue perfusion (40-70%)
Initiated by gram-negative (most common) or
gram positive bacteria, fungi, or viruses
infection enters bloodstream and is carried
throughout body
Toxins released overcome compensatory
mechanisms
Can cause dysfunction of one organ system or
cause multiple organ dysfunction
The syndrome of septic shock is characterized by
Systemic vasodilation (hypotension)
Diminished myocardial contractility
Widespread endothelial injury and activation
leading to fluid leakage (capillary leak) resulting in
acute respiratory distress syndrome (ARDS)
Activation of the coagulation cascade leading to
disseminated intravascular coagulation.
Clinically presents in two phases:
“Warm” shock - early phase
hyperdynamic response, Vasodilation
Pink, warm, flushed skin
Increased Heart Rate
Tachypnea
Massive vasodilation
“Cold” shock - late phase
hypodynamic response, Decompensated state
Vasoconstriction
Skin is pale & cold
Tachycardia
Decrease BP
Metabolic and respiratory acidosis with hypoxemia
Neurogenic shock
A type of distributive shock that results from the
sudden loss or suppression of sympathetic tone
or vasomotor tone
Causes massive vasodilatation in the venous
vasculature, leading to venous return to heart
and cardiac output.
Occurs in
Deep general anesthesia
Spinal injury
Brain damage
Pathophysiology
Loss of sympathetic tone (parasympathetic response)
results in massive vasodilatation, inhibition of the
baroreceptor response, and impaired thermo-regulation.
Arterial vasodilatation drop in BP
Decrease in BP & drop in CO impaired tissue perfusion.
Inhibition of baroreceptors no reflex
tachycardia, further compromising tissue perfusion
Psychogenic shock
It is a mental state resulting from an unpleasant
experience generating a vasovagal response
Stages of Shock
Initial non-progressive stage Baro-receptor reflexes
Release of catecholamine
Activation of renin-angiotensin-aldosteron system
ADH release
results in tachycardia, peripheral vasoconstriction (cool skin) and renal fluid conservation
Progressive stage Widespread tissue hypoxia results in anaerobic glycolysis and
Lactate acidosis (pH < 7.35)
Vasodilation with blood pooling in microcirculation
Declined cardiac output
Oligouria
Widespread tissue hypoxia
Irreversible stageWidespread cell injury leading to
Further decreased myocardial contractility
Anuria with tubular necrosis
Ischemic bowl may lead to leakage of bacterial flora
Fluid lung (ARDS)
Postmortem changes
Brain
Show ischemic encephalopathy with initial sweeling
or shrinkage of neurons later nerve cells die and are
replaced by fibrillary gliosis
Kidneys
Ischemia leads to Acute Tubular Necrosis (ATN)
Can be normal in size or enlarged
If extensive muscle injury, peculiar brown tubular
casts are seen
GI tract
The GI tract is at very high risk of infarction. Shock
causes infarction of the GI epithelium
Liver
Fatty changes may be seen
Centrilobular necrosis is common.
Heart
Grossly, subendocardial hemorrhages are
common.
Microscopically, contraction bands are seen in
myocardial cells.
Fatty change – 18 to 24 hrs well marked in 3 to 4
days
Lung
Shock causes release of inflammatory mediators
such as TNF-α. This injures endothelial cells.
Endothelial injury allows leakage of proteinaceous
fluid and neutrophils into the interstitium.
interstitial edema and inflammation common in
shock.
Edema is well discernible after 2 to 3 days
Lungs become heavy, stiff, and hemorrhagic.
Medicolegal Importance
In a person with hemorrhagic diathesis or hemophilia, minor injury produce death from hemorrhage.
Sudden rise of BP in neurogenic shock can precipitate serious complications like –
(a) Intracerebral hemorrhage from rupture of arteriosclerotic cerebral vessels or of berry aneurysm.
(b) Rupture of a dissecting aneurysm of aorta.
Under such conditions even when the deceased received minor trauma before death, the essential cause of death will be underlying disease process.
Minor stimuli or injury over receptic spots may cause sudden death from neurogenic shock.
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