Understanding Shock: Types, Causes, and Treatment

• Shock is a life-threatening condition from inadequate tissue perfusion, leading to cell dysfunction and death.
• Multiple organ dysfunction syndrome (MODS) can result from untreated shock, especially septic shock.
• Rapid assessment and early intervention are critical for patient recovery.

Overview of Shock

• It's a clinical syndrome due to inadequate tissue perfusion, causing imbalance between oxygen and nutrient delivery and cellular function
• Effective cardiac pump, adequate vasculature, and sufficient blood volume are needed for adequate blood flow.
• Without treatment, cells experience hypoxia, leading to organ dysfunction and death.
• Shock affects all body systems and can develop rapidly or slowly based on the cause.
• The body activates homeostatic mechanisms to restore blood flow during shock.
• Any patient with any disease is at risk of shock.
• Shock is classified by its underlying cause, such as hypovolemic, cardiogenic, or distributive.
• Common responses to all types of shock: hypoperfusion, hypermetabolism, and inflammatory response.
• Failure of compensatory mechanisms leads to end-organ dysfunction and death.
• Nursing care requires systematic assessment and collaboration with the healthcare team.
• Nurses need to identify early signs of shock for rapid therapy.

Normal Cellular Function

• Energy metabolism breaks down nutrients into adenosine triphosphate (ATP).
• ATP fuels processes like active transport, muscle contraction, biochemical synthesis, and electrical impulse conduction.
• Aerobic metabolism is more efficient for ATP production than anaerobic metabolism.
• Anaerobic metabolism produces lactic acid, which must be converted by the liver.

Pathophysiology

• Shock involves cellular changes, vascular responses, and blood pressure changes.

Cellular Changes

• Cells lacking oxygen and nutrients use anaerobic metabolism.
• This results in low-energy yields and an acidic intracellular environment.
• Cell function stops; it swells, and the membrane becomes permeable.
• The sodium-potassium pump is impaired, cell structures are damaged, and cell death occurs.
• Glucose is needed for ATP production.
• Stress states release catecholamines, cortisol, glucagon, and cytokines.
• This causes hyperglycemia and insulin resistance to mobilize glucose.
• Gluconeogenesis (glucose formation from non-carbohydrates) is promoted.
• Glycogenolysis converts stored glycogen to glucose, increasing blood glucose.
• Continuous stress response depletes glycogen, increasing proteolysis and organ failure.
• Nutrient and oxygen deficits cause a buildup of metabolic end products.
• The clotting cascade is activated, leading to small clots in microcirculation.
• This further compromises tissue perfusion.
• Cellular metabolism is impaired, initiating a negative feedback loop.

Vascular Responses

• Local regulatory mechanisms (autoregulation) cause vasodilation or vasoconstriction.
• They respond to biochemical mediators released by cells.
• Cytokines trigger action at a cell site or travel to distant sites.
• Researchers are learning about the physiologic actions of biochemical mediators in shock.

Blood Pressure Regulation

• Blood volume, cardiac pump, and vasculature maintain blood pressure and perfuse tissues.
• Blood pressure is regulated by neural, chemical, and hormonal feedback systems.
• Mean arterial pressure (MAP) must exceed 65 mm Hg for cells to metabolize energy.
• MAP = Cardiac output x Peripheral resistance
• Cardiac output depends on stroke volume and heart rate.
• Peripheral resistance depends on arteriole diameter.
• Baroreceptors in the carotid sinus and aortic arch monitor circulatory volume.
• When blood pressure drops, catecholamines increase heart rate and cause vasoconstriction.
• Chemoreceptors regulate blood pressure and respiratory rate in response to oxygen and carbon dioxide levels.
• Kidneys regulate blood pressure by releasing renin, which leads to angiotensin II (a vasoconstrictor).
• Aldosterone is released, promoting sodium and water retention (hypernatremia).
• Antidiuretic hormone causes kidneys to retain water to raise blood volume and blood pressure.

Stages of Shock

• Shock progresses along a continuum and can be early or late based on organ dysfunction.
• The stages: compensatory (stage 1), progressive (stage 2), and irreversible (stage 3).
• Earlier intervention increases the chance of survival.
• Current research focuses on early, aggressive interventions to reverse tissue hypoxia.
• Aggressive therapy within 3 hours of identifying shock increases survival, especially in septic shock.

Compensatory Stage

• Blood pressure remains normal.
• Vasoconstriction, increased heart rate, and increased contractility maintain cardiac output.
• Sympathetic nervous system stimulates catecholamine release.
• The body shunts blood to the brain, heart, and lungs. Skin may be cool and pale, bowel sounds are hypoactive, and urine output decreases.
• Inadequate perfusion leads to anaerobic metabolism and lactic acid buildup, causing metabolic acidosis.
• Respiratory rate increases to increase oxygen and compensate for acidosis.
• Rapid breathing removes excess carbon dioxide, causing respiratory alkalosis.
• The patient may be anxious or confused.
• Treatment in this stage improves the prognosis.

Progressive Stage Characteristics

• Systolic blood pressure ≤100 mm Hg or MAP ≤65 mm Hg
• Requires fluid resuscitation to support blood pressure
• Heart rate >150 bpm
• Rapid, shallow respirations; PaCO2 increases; hypoxemia
• Change in mental status
• Serum lactate >4 mmol/L
• Urine output <0.5 mL/kg/h

Management Strategies

• Fluid resuscitation with crystalloid solutions (minimum initial bolus of 30 mL/kg)
• Vasopressor agents (e.g., norepinephrine) if hypotension persists
• Respiratory support with supplemental oxygen or mechanical ventilation
• Blood transfusions for low hemoglobin