Introduction
Failure of the normal regulatory mechanisms in the body can lead to rapid and profound shock. Shock can be defined as a state of inadequate perfusion relative to tissue demands. In part one of this article, you will review the pathophysiology of shock. Next month in part two, you’ll learn about cardiogenic, hypovolemic, anaphylactic, and neurogenic shock. Part two also includes a brief review of sepsis and septic shock.
Classification
There are three major classes of shock:
• Cardiogenic: loss of an efficient cardiac pump
• Hypovolemic: inadequate blood volume
• Distributive (neurogenic, anaphylactic, and septic): an unhealthy vascular bed, resulting in a mismatch between blood volume and the size of the vascular bed
The cascading events of shock begin with inadequate oxygen transport and cellular dysfunction, which proceed to tissue and vascular disturbances, and end with organ dysfunction or failure.
Pathophysiology of Shock
1. Initial Stage of Shock
This is the stage in which there are cellular changes in response to shock. Diminished blood flow to the microcirculation reduces oxygen delivery and sequesters metabolic by-products, thereby reducing oxygen delivery and utilization. The cell metabolism suffers, and the cell begins to deteriorate. There are also no clinical signs or symptoms except elevated lactate levels.
2. Compensatory Stage of Shock
The homeostatic compensatory mechanisms of the body are activated by decreased cardiac output. Compensation is mediated through neural, hormonal, and chemical changes.
Neural Compensation
Baroceptors located in the aorta and carotid bodies sense a decrease in the blood pressure. This causes stimulation of the sympathetic nervous system. Epinephrine and norepinephrine are released from the adrenal medulla, to:
1. Constrict the blood vessels in the skin, GI tract and kidneys
2. Dilate the blood vessels in the skeletal muscles and coronary arteries
3. Sweat
4. Increase the heart rate and contractility
5. Increase the rate and depth of breathing
6. Dilate the pupils
Hormonal Compensation
Mediated through the sympathetic nervous system, humoral compensation begins. The anterior pituitary releases ACTH, which causes a release of mineralocortocoids and glucocorticoids. The mineralocorticoids balance the sodium and water levels. The glucocorticoids regulate the metabolic function of the body through the stress response.
The posterior pituitary releases ADH, causing vasoconstriction and renal retention of water.
The kidneys, which are flow dependent, also sense the decreased blood pressure. The kidneys release renin in response, which then stimulates the angiotensin and aldosterone systems. These hormones cause:
1. Retention of sodium and water
2. Increased blood volume in the major blood vessels because of water retention and vasoconstriction of the smaller blood vessels
3. Decreased urine volume and sodium excretion
4. Increased potassium excretion and increased urine osmolarity
Chemical Compensation
Hypoxemia and cellular hypoxia cause an increase in respiratory depth and rate. The acid-base balance is disturbed with the "blowing off" of CO2, which leads to respiratory alkalosis. The combination of hypoxemia and alkalosis adversely affects the level of consciousness.
3. Progressive Stage of Shock
In this stage of shock, previously helpful compensatory responses are no longer effective. Severe hypoperfusion to all organ systems causes multi-organ dysfunction syndrome (multi-system organ failure). The microcirculation loses the ability to autoregulate blood flow, leading to decreased blood volume returning to the central blood vessels. This causes further organ hypoperfusion.
4. Refractory Stage of Shock
This final and irreversible stage reflects the very last part of a patient’s life. The cellular and organ destruction has been so severe that death is inevitable.
Essential versus Non-essential Organs
The body long ago developed a priority list for when there is a decreased amount of blood available. On the top of the list:
• Brain
• Heart
• Lungs
These organs will receive the most blood possible during shock through stimulation of the beta receptors, which causes vasodilation.
The other organs of the body, such as the skin and gut are considered to be "non-essential organs."
Organ-Specific Effects of Shock
Brain - Essential Organ
Beta adrenergic stimulation dilates cerebral vessels to attempt to maintain enough flow for a MAP of 50. Late in shock, the vasomotor center fails to recognize and respond to sympathetic stimulation. Early symptoms of hypoperfusion are irritability and agitation, replaced by unresponsiveness in late stages.
Heart - Essential Organ
In all forms of shock except cardiogenic shock, the myocardium experiences a protective flow. Autoregulation maintains coronary flow as long as arterial pressure does not fall below 70 mm/Hg. The deterioration of heart function makes shock irreversible.
All other organs are considered biologically expendable.
Skeletal Muscle, Fat, Skin
Vasoconstriction from alpha receptor stimulation results in muscle weakness, cramping, and fatigue. The skin becomes cool; its color ashen to cyanotic. The potential for skin breakdown is enormous.
Kidneys
The low blood pressure is seen as a decreased glomerular filtration rate (GFR) by the kidney. In order to increase flow, the kidneys activate the renin-angiotensin-aldosterone compensatory mechanism. Metabolic acidosis is perpetuated by the kidneys’ inability to break down and excrete lactic acid.
Lungs
Hyperpnea occurs as a compensatory response to sympathetic stimulation, hypoxia, and metabolic acidosis. The increased respiratory rate increases pulmonary muscle oxygen consumption. Coupled with primary damage from centrally mediated chemicals to pulmonary capillary endothelial cells, the increased capillary permeability results in interstitial and intra-alveolar edema and decreased pulmonary compliance. Resultant decreased ventilation and impeded gas exchange further decrease oxygen delivery to cells.
Mesentery
In early stages of shock, there is a marked decrease in blood flow to the gut manifested by nausea, vomiting, and hypoactive bowel sounds. Later, intestinal damage and necrosis by digestive enzymes cause damage to the protective mucosal barrier. Bacteria and toxins are released into the bloodstream.
Liver
The metabolic rate of the liver is very high with consumption of large quantities of oxygen and nutrients. In shock, the catecholamines stimulate liver activity. Glucose is made available to the cells, which are unable to use it, resulting in hyperglycemia. Hepatic ischemia results in a decrease in its metabolic and detoxification functions. Loss of clotting factors induce coagulopathies such as DIC.
Pancreas
Shock induces the release of amylase and lipase into the circulation. A chemical called myocardial depressant factor (MDF), released from the pancreas, decreases myocardial contractility.
Conclusion
Patients with a wide variety of problems can develop shock. You’ve reviewed what the stages of shock are and the effects of shock on the organs of the body. Knowing the underlying pathophysiology may help guide you in assessing and managing the care of the patient with shock. Next month in part two, we’ll discuss cardiogenic, hypovolemic, anaphylactic, neurogenic and septic shock in greater detail.
Some of the material in this article was excerpted from the Shock and Infection in Critical Care Primer offered by TCHP. The TCHP Education Consortium offers homestudy education on a variety of health care topics on their website at www.tchpeducation.com. Homestudies are available to read free of charge on their website. If contact hours are desired, the processing cost is $5 per contact hour.
References
http://www.nlm.nih.gov/medlineplus/ency/article/003133.htm accessed 07.24.08
