PCT - Bleeding and Shock 2

Hyperperfusion and Shock

• Definition of Hyperperfusion: Occurs when tissue perfusion levels decrease below normal, leading to inadequate blood flow to cells and failure to eliminate metabolic waste.

• Shock: A state of collapse and failure of the cardiovascular system, resulting in inadequate circulatory and tissue perfusion. Not a specific disease, but can manifest in various forms of shock.

• Symptoms of Early Shock: Subtle changes often occur before vital signs appear abnormal, emphasizing the need for early evaluation of organ perfusion.

• Consequences of Unaddressed Shock: Failure to address shock leads to rapid deterioration of the patient, emphasizing the need for timely intervention.

Mechanisms of Shock

• Intact Mechanisms Needed for Perfusion: Requires functioning heart, blood vessels, and adequate blood volume.

• Types of Shock:

  • Cardiogenic Shock: Results from the heart's failure to pump effectively due to conditions like myocardial infarction or severe arrhythmias.

  • Hypovolemic Shock: Most common type, typically due to loss of blood volume from hemorrhagic events or dehydration. Treatment focuses on addressing hypovolemia.

  • Neurogenic Shock: Caused by failure of the sympathetic nervous system to maintain vascular tone, often resulting from spinal cord injuries.

Compensation Mechanisms for Decreased Perfusion

• Baroreceptors: Located in the aortic arch, these pressure sensors react to blood pressure changes, stimulating compensatory vasoconstriction through the sympathetic nervous system.

• Renin-Angiotensin-Aldosterone System (RAAS): Activated in response to hypoperfusion, promoting salt and water retention, vasoconstriction, and increased blood pressure.

• Hormonal Response: Release of epinephrine and norepinephrine enhances heart rate, contraction strength, and peripheral vascular resistance to improve cardiac output.

Types of Shock: Detailed Discussion

• Cardiogenic Shock:

  • Caused by inadequate heart function, most commonly following significant myocardial infarction.

  • Poor prognosis if more than 40% of the left ventricle is dysfunctional, with mortality rates up to 80% even with treatment.

• Hypovolemic Shock:

  • Resulting from external or internal fluid loss. Commonly seen in traumatic injuries.

  • Symptoms include pale, cool, clammy skin, increased heart rate, and low blood pressure.

• Neurogenic Shock:

  • Often associated with spinal cord injuries, leading to widespread vasodilation and relative hypovolemia.

  • Symptoms may include warm, dry skin below the injury level.

• Distributive Shock: Includes septic, neurogenic, and anaphylactic shock, characterized by widespread vasodilation.

  • Septic Shock: Often leading to multiple organ dysfunction syndrome (MODS), caused by severe infections triggering systemic inflammatory responses.

  • Anaphylactic Shock: Severe allergic reaction resulting in vasodilation and bronchoconstriction; treated with epinephrine.

Cellular Metabolism and Consequences of Shock

• Cellular metabolism becomes impaired and anaerobic respiration leads to lactic acid accumulation.

• This results in metabolic acidosis, decreased ATP production, cellular edema, and compromised cellular function.

• Accumulation of metabolic waste products exacerbates tissue hypoxia and contributes to further organ dysfunction.

SIRS and Sepsis

• SIRS (Systemic Inflammatory Response Syndrome): A clinical syndrome indicating potential infection, characterized by fever/hypothermia, tachycardia, tachypnea, and abnormal white blood cell counts.

• Criteria for SIRS: Requires two or more of the following:

  • Temperature >38°C or <36°C

  • Heart rate >90 bpm

  • Respiratory rate >20 breaths/min or CO2 <32 mmHg

  • White blood cell count >12,000 or <4,000 or >10% bands.

Clinical Indicators and Treatment Protocols

• Assessment of Shock: Evaluating vital signs, mental status, peripheral perfusion (capillary refill), and history of bleeding/injury.

• IV Fluid Therapy: For shock management, normal saline is commonly used for fluid resuscitation, while monitoring for fluid overload is critical.

• Transport Considerations: Shorten on-scene time in critically ill patients; prioritize transport to medical facilities for definitive care.

• Emergent Treatments: Epinephrine for anaphylactic shock, fluid resuscitation for hypovolemic shock, and early intervention for suspected septic shock are crucial.

Management Strategies

• Positioning the patient (e.g., Trendelenburg) and preventing hypothermia during transport.

• Objectives for severe shock: Restore blood pressure, maintain perfusion, and begin early treatment in line with transport protocols.

• Future Directions in Shock Management: Integration of immediate care protocols and innovative treatment devices for cardiac and trauma patients.