Hemorrhagic Shock

Musa Aminu Muhammad

Outline
• Introduction
• Etiologic Types of shock
• Hemorrhagic Shock
• Epidemiology
• Pathogenesis
• Morphology
• Clinical manifestations
• Management
• Prognosis
• Conclusion
Introduction
• Shock is a state of circulatory failure that impairs tissue
perfusion and leads to cellular hypoxia.
• It can be defined as a state of systemic tissue hypo perfusion
resulting from reduced cardiac output and/or reduced effective
circulating blood volume, and/or increase vasodilation.
Etiologic Types of Shock
Shock can be classified based on etiology and this causes fall
into three general categories, namely:
• Cardiogenic
• Hypovolemic
• Septic
• Neurogenic
• Anaphylactic
Types Cont.
Other classification include:
• Cardiogenic (pump failure)
• Hypovolemic (volume failure)
• Distributive (Capacity failure)
• Obstructive (Lumen failure)
Hypovolemic shock is caused by a critical decrease in
intravascular volume.
What is Hemorrhagic Shock??
• Hemorrhagic Shock is a type of hypovolemic shock that is due to
loss of blood.
• Common causes of bleeding (hemorrhagic shock), typically include:
• Trauma
• surgical interventions
• peptic ulcer
• esophageal varices
• ruptured aortic aneurysm.
• Bleeding may be overt (eg, hematemesis, melena) or concealed (eg,
ruptured ectopic pregnancy).
Hemorrhagic Shock
• Bleeding may also be internal (e.g Hemothorax, hemopritoneum)
or external (e.g. Trauma, GI bleeding etc).
• Hypovolemic shock can be due to other causes aside
hemorrhage which include:
1. Loss of plasma(e.g from burns surface, exfoliative dermatitis)
2. Loss of fluid and electrolyte (e.g. diarrhea, vomiting, polyuria,
ascites)
• Bleeding the commonest cause of hypovolemic shock.
Epidemiology
• Trauma remains a leading cause of death worldwide with
approximately half of these attributed to hemorrhage.
• In the United States in 2001, trauma was the third leading cause
of death overall, and the leading cause of death in those aged 1
to 44 years. Wikipedia)
• While trauma spans all demographics, it disproportionately
affects the young with 40% of injuries occurring in ages 20 to 39
years by one country's account. Of this 40%, the greatest
incidence was in the 20 to 24-year-old range.
Epidemiology Cont.
• Hemorrhagic shock is tolerated differently, depending on the
preexisting physiologic state and, to some extent, the age of the
patient.
Very young and very old patients are more prone to early
decompensation after loss of circulating blood volume.
Pathogenesis
• Septic shock may be more proinflammatory than other forms of
shock because of the actions of bacterial toxins, especially
endotoxin.
• Blood pressure is not always low in the early stages of shock
(although hypotension eventually occurs if shock is not reversed).
• The process of arterial contraction due to fall in blood volume is
known as reverse stress relaxation of the circulatory system.
• Clotting mechanisms are immediately activated
Stages of Shock
• Shock is a progressive disorder that leads to death if the underlying
problems are not corrected
• Shock tends to evolve through three general stages. These stages have
been documented most clearly in hypovolemic (e.g. hemorrhagic) shock
but are common to other forms as well:
1. An initial nonprogressive stage during which reflex compensatory
mechanisms are activated and vital organ perfusion is maintained
2. A progressive stage characterized by tissue hypoperfusion and onset of
worsening circulatory and metabolic derangement, including acidosis
3. An irreversible stage in which cellular and tissue injury is so severe that
even if the hemodynamic defects are corrected, survival is not possible
Nonprogressive Stage
• Various neurohumoral mechanisms help maintain cardiac output
and blood pressure.
• MAP=CO×TPR
• These mechanisms include:
1. baroreceptor reflexes
2. release of catecholamines and antidiuretic hormone
3. activation of the renin-angiotensin-aldosterone axis
Baroreceptor Reflex
Carotid Sinus and Carotid Body
• The carotid body contains chemoreceptors and is involved in
both respiratory and cardiovascular control through complex
neural pathways. Its most essential function is the reflex
adjustment of respiration according to the arterial blood gas
values.
• Carotid sinus contains baroreceptors.
Baroreceptor Reflex
Sympathetic Stimulation
• Epinephrine and Norepinephrine has chronotropic, dromotropic,
and inotropic effect on the heart which results in increased HR
and cardiac contractility.
• Catecholamines causes venoconstriction and
arterioloconstriction resulting in increased preload (end
diastolic blood pressure) and TPR respectively.
• MAP=CO×TPR
• Results in increased systolic and diastolic blood pressure
Exceptions
• The internal carotid and coronary arteries are exceptionally and
relatively resistant to the vasoconstrictive effect of the
sympathetic SANS
• This forms the basis of blood redistribution from other organs
to the more vital organs especially the heart and brain.
• Blood supply to the skin, GIT, and kidney is especially
compromised at this stage.
• However renal blood flow compromise at this stage is
somewhat beneficial.
Renin Angiotensin Aldosterone Axis
• Reduced renal perfusion and sympathetic stimulation causes the release of renin
which then converts angiotensinogen into Angiotensin I.
• Angiotensin I upon passing through the pulmonary circulation is converted to
Angiotensin II by ACE.
1. Ang II can induce thirst by stimulating the subfornical area. The subfornical
organ resides just under the fornix and is active in many bodily processes,
including osmoregulation.
2. Angiotensin II is a strong vasoconstrictor and hence causes venoconstriction
and arterioloconstriction thereby further stabilizing systolic and diastolic blood
pressure.
3. Stimulation of Angiotensin receptors on zona glomerulosa cells of the adrenal
cortex results in the synthesis and release of aldosterone. However this takes
longer time.
Renin Angiotensin Aldosterone Axis.
• Aldosterone acts on the principal cells of the nephron to cause
salt and water retention which in turn enhances blood volume.
• Increase in blood volume increases CO
Vasopressin (ADH)
• Baroregulation of vasopressin secretion in response to
hypovolemia or hypotension is by far the most important of the
nonosmotic stimuli.
• Vasopressin acts on the terminal nephron to cause water
reabsorption
• High concentration of ADH also causes arterioloconstriction
and consequently enhancing diastolic blood pressure by
increasing TPR
Fluid Shift
• There is considerable shifting of interstitial fluid and electrolyte
into the because of decreased hydrostatic pressure which may
result in further fluid and electrolyte imbalance and cellular
shrinkage
Progressive Stage

• If the underlying causes are not corrected, shock passes

imperceptibly to the progressive phase, which as noted is
characterized by widespread tissue hypoxia.
• Hypoxia causes a switch in cellular respiration from aerobic
oxidative phosphorylation to anaerobic glycolysis, the end
product of which is lactic acid. => Lactic acidosis
• Lactic acid is a vasodilator and cardiodepressor
Positive Vicious Circle
• Endothelial damage further leads to NO release into the
circulation.
• Waste products such as CO2 accumulates
• Lactic acid, NO, and CO2 lead to further vasodilation and
depression of the cardiac tissue.
• Vasodilation and cardiac depression in turn lead to decrease CO
and TPR which result in severe crippling of Mean Arterial Pressure
and the mechanisms that regulate it. The vicious circle sets in.
• These substances also depress the vasomotor center, reducing
the sympathetic outflow and constriction mechanism failure.
Irreversible Stage
• In the absence of appropriate intervention, or in severe cases, the
process eventually enters an irreversible stage characterized by:
• Widespread cell injury due to chronic ATP depletion, membrane damage,
lysosomal leakage, and mitochondrial damage in various tissues.
• In the absence of appropriate intervention, or in severe cases, the
process eventually enters an irreversible stage.
• The ischemic bowel may allow intestinal flora to enter the circulation,
and thus bacteremic shock may be superimposed.
• Renal failure.
• DIC due to blood stasis
Morphology
GIT
• Prolonged ischaemia to the GIT will manifest as multiple patchy
mucosal necrosis which will result in bacterial shift to the
circulation leading to superimposed bacteremia and septic shock.
Others
• Although any organ can be affected, the brain, heart, kidneys, adrenals,
and gastrointestinal tract are most commonly involved.
• Fibrin thrombi can form in any tissue but typically are most readily
visualized in kidney glomeruli.
Morphology
• Adrenal cortical cell lipid depletion is akin to that seen in all forms of
stress and reflects increased use of stored lipids for steroid
synthesis.
• Other tissues may recover if the patient survives except cardiac and
neuronal cells.
At autopsy:
• Liquefactive necrosis in the brain
• MI in the heart
• Fatty change in perivenular cells of the liver and/or hepatocyte
necrosis
• Micro necrosis on the GI mucosal lining.
Clinical Features
• Hypotension
• Weak rapid pulse
• Tachypnea
• Cool, clammy, cyanotic skin
Prognosis
• More than 90% of young, otherwise healthy patients with
hypovolemic shock survive with appropriate management; by
comparison, septic or cardiogenic shock is associated with
substantially poorer outcomes, even with state-of-the-art care.
Reference
• Robbins Pathologic Basis of Disease. 10th edition
• Shock – Critical Care Medicine – MSD Manual Professional
Edition. https://www.msdmanuals.com/professional/critical-
care-medicine/shock-and-fluid-resuscitation/shock
• Hemorrhagic Shock – Medscape. https://emedicine.medscape.
com/article/432650-overview?
icd=login_success_email_match_norm#a4
• Dr Najeeb.