Lecture on Shock

May 24, 2024

Lecture on Shock by Eddie Watson

Introduction

  • Presenter: Eddie Watson
  • Series: Lessons on Shock
  • Focus: Basics of shock and physiological response

What is Shock?

  • Circulatory Shock: Differentiates from psychological fright or post-traumatic events.
  • Classical Definition: Acute, widespread reduction in effective tissue perfusion; leads to oxygen supply and demand imbalance, anaerobic metabolism, lactic acidosis, cellular and organ dysfunction, and possible death.
  • Core Concept: Decreased tissue perfusion resulting in less oxygen delivery than demand.
    • Formula: O2 Delivery < O2 Demand

Key Consequences of Shock

  • Oxygen Delivery: Decreased blood leads to decreased oxygen delivery.
  • Cell Death: Leads to organ failure and possibly death if prolonged.
  • Life-Threatening Condition: Emphasis on urgency and severity.

Physiological Response to Shock

Anatomy Involved

  • Heart: SA node, AV node, bundle of His, Purkinje fibers—control electrical conduction.
  • Vasculature: Aorta, branches, baroreceptors, and chemoreceptors located in the aortic arch and carotid sinuses.
  • Brain: Medulla oblongata, pituitary gland.
  • Kidneys: Adrenal gland atop.

Hypoperfusion Effects

  • Aerobic vs. Anaerobic Metabolism:
    • Aerobic -> ATP from oxygen in electron transport chain.
    • Anaerobic -> Less ATP, cell death, lactic acid accumulation.
  • Metabolic Acidosis: Result of lactic acid and CO2 buildup.

Physiological Responses

  • Decreased Mean Arterial Pressure (MAP): Leads to reduced baroreceptor firing.
  • Medulla Responses:
    • Cardio Regulatory Center: “Cardio-inhibitory” (lowers heart rate) and “Cardio-acceleratory” (increases heart rate and stroke volume).
    • Vasomotor Center: Activates sympathetic responses -> adrenaline and noradrenaline release, causing vasoconstriction.
  • Renin-Angiotensin-Aldosterone System (RAAS):
    • Renin: Produced by the adrenal gland; interacts with angiotensinogen from the liver to form angiotensin I, then angiotensin II (lung enzyme “ACE” catalyzes conversion).
    • Angiotensin II: Increases thirst, vasoconstriction, and triggers aldosterone release, leading to sodium and water reabsorption -> increased intravascular volume and MAP.
  • Antidiuretic Hormone (ADH): Released from pituitary due to increased sodium, enhances water reabsorption to increase MAP.

Signs and Symptoms of Shock

  • Decreased Blood Pressure: Common sign.
  • Increased Heart Rate: Usually present except in one form of shock.
  • Weak and Thready Pulse
  • Rapid, Shallow Breathing
  • Pallor
  • Absent or Decreased Bowel Sounds
  • Signs of End Organ Damage:
    • Confusion, lethargy
    • Reduced/absent urine output
    • Cold, clammy, mottled skin
    • ST elevation in ECG

Lab Findings in Shock

  • Elevated Lactate: From anaerobic metabolism.
  • Decreased pH: Indicates metabolic acidosis.
  • Elevated BUN and Creatinine
  • Elevated ALT and AST: Indicates liver damage (shock liver).
  • Elevated Troponin
  • Decreased PaO2: Less oxygen in the blood.
  • Altered SvO2: Can be elevated or decreased depending on shock type.

Conclusion

  • Summary: Basics of shock, physiological response, and signs/labs of shock.
  • Next: Lessons on stages of shock and causes.
  • Call to Action: Like, subscribe, ask questions, and watch next lesson or hemodynamic series.