Path Day 2: Shock

Understanding Shock

• Definition: Shock is defined as hypoperfusion, which means inadequate blood flow to tissues.

• Perfusion: Good perfusion is essential for homeostasis, meaning tissues receive adequate oxygen and glucose for aerobic metabolism.

• Hypoperfusion: It leads to cells not receiving sufficient blood flow, resulting in tissue damage.

Causes of Shock

• Hydrostatic Pressure: A central term to understand!

  • Low blood pressure reduces hydrostatic pressure, causing hypoperfusion.

  • Measurement: Mean Arterial Pressure (MAP) is crucial; normal MAP is ≥65 mmHg in adults.

    • In children: The formula is 70 + (2 x age) in years.

    • Ex: A 4-year-old should have a systolic BP ≥78 mmHg.

MAP Calculation Detour

• Terms to know:

  • Pulse pressure, which is the difference between systolic and diastolic blood pressure.

• Example: If systolic is 110 and diastolic is 86:

  • Calculation: 110 - 86 = 24 (Pulse Pressure)

• Calculating Mean Arterial Pressure (MAP)

  • Definition: MAP is an important cardiovascular measure that reflects the average blood pressure in a person's arteries during one cardiac cycle.

    • Calculation Steps:

      1. Calculate the pulse pressure (subtract the systolic number from the diastolic number) - in this example, 24

      2. Divide the pulse pressure by 3:

         • Example: 24 / 3 = 8

      3. Add this value to the diastolic pressure:

         • Example: 86 + 8 = 94 (Mean Arterial Pressure)

Consequences of Hypoperfusion

• Cellular Effects:

  • Leads to hypoxia and a shift toward anaerobic metabolism.

  • Anaerobic metabolism yields only 2 ATP compared to 38 from aerobic metabolism.

  • This process produces lactic acid, causing metabolic acidosis with a pH below 7.35.

• Lactate Levels: Normal is below 1 mmol/L; levels above 2 mmol/L indicate stress, while 4-5 mmol/L suggest severe shock.

Cellular and Systemic Responses to Shock

• Sodium-Potassium Pump Dysfunction:

  • In shock, reduced ATP disrupts the pump, causing sodium to accumulate intracellularly, leading to cellular swelling.

• Symptoms of Shock:

  • Tachycardia (increased heart rate), bradycardia (in some cases), hypertension, anxiety, respiratory difficulties, clammy skin, and thirst due to low perfusion.

Body's Response to Low Perfusion

• Baroreceptors detect low blood pressure and signal the brain.

• Hormonal Response:

  • Sympathetic nervous system activation leads to release of catecholamines (e.g., epinephrine, norepinephrine).

  • Renin Angiotensin Aldosterone System (RAAS) activates to maintain BP through vasoconstriction (angiotensin II) and sodium retention (aldosterone).

  • ADH is also released to conserve fluids.

Catecholamines and Their Effects

• Epinephrine:

  • Beta 1: Increases heart rate (chronotropic effect - think chrono = time), force of contraction (inotropic effect), and conduction speed in the heart (dromotropic effect - controls electricity to heart).

  • Beta 2: Causes bronchodilation and vasodilation in essential areas (like muscles and heart).

  • Alpha 1: Causes vasoconstriction, increasing blood pressure.

• Norepinephrine: Primarily acts as an alpha 1 agonist, leading to significant vasoconstriction to improve BP.

Mechanisms for Increasing Blood Pressure

• Constriction of blood vessels** increases hydrostatic pressure to improve perfusion.

• Attention to Urine Output: Decreased urine output often indicates poor renal perfusion, a sign of shock.

• Assessment: Recognize vital signs and monitor lactate levels to evaluate shock severity.

Signs and Symptoms of Shock

• Cognitive & Physical Indicators:

  • Anxiety/agitation due to catecholamine activation.

  • Rapid weak pulse, clammy pale skin.

  • Shortness of breath, tachycardia, and GI issues (nausea and vomiting) due to reduced blood flow.

  • Delayed cap refill indicating poor perfusion.

• Organ Sensitivity: Heart and brain can only survive 4-6 minutes without oxygen. Kidneys and liver can last 30-60 minutes. Bones and Muscle can last anywhere from 12-24 hours.

• MODS stand for Multiple Organ Dysfunction Syndrome, which occurs when two or more organ systems fail due to inadequate oxygen delivery.

Body's Response to Shock

• Other mechanisms exist for the body to manage shock besides medications such as calcium channel blockers. These include compensatory responses like increased heart rate, vasoconstriction, and the release of stress hormones to maintain blood flow to vital organs.

• Constriction may not solely depend on alpha or beta receptors. Instead, other factors such as local tissue hypoxia and inflammatory mediators can also play a significant role in regulating vascular tone and promoting compensatory mechanisms - the activation of RAAS contributes to fluid retention and increased blood pressure, further supporting the body's attempt to counteract the effects of shock.

Stages of Shock

• Compensated Shock:

  • Defined as when the body maintains blood pressure sufficiently for perfusion despite losing blood.

  • Observable signs include tachycardia and an acceptable blood pressure to sustain perfusion.

  • Example: A patient from a motor vehicle collision (MVC) with a heart rate of 130 and blood pressure of 118/70 is in compensated shock.

  • Compensation Mechanism:

    • The body releases catecholamines (epinephrine and norepinephrine) to increase heart rate and blood pressure.

• Decompensated Shock:

  • Occurs when blood pressure drops below the level necessary to sustain perfusion.

  • Marked by a mean arterial pressure (MAP) below 65 for adults or a systolic blood pressure below 70 +2x age for children.

Compensatory Mechanisms in Shock

• Compensated shock involves significant catecholamine release!

  • Removal of these hormones, such as during Rapid Sequence Intubation (RSI) using paralytics and sedatives, can critically impair the patient.

  • Medications like beta blockers could hinder the compensation mechanism in patients who typically rely on catecholamines to maintain blood pressure.

Renin-Angiotensin System Interaction

• In shock, the body activates RAAS, leading to sodium retention, ultimately increasing blood pressure through vasoconstriction.

• Factors Influencing Compensation:

  • Elderly patients may struggle with shock due to pre-existing conditions and medications like ACE inhibitors and beta blockers.

Types of Shock

• Shock can primarily be categorized into two categories, central and peripheral.

Central Shock

1. Cardiogenic Shock:

   • Caused by inadequate cardiac output (pump failure).

   • The most common cause is a myocardial infarction (MI).

   • Other causes include tachyarythmias and bradyarythmias, valve disfunction or rupture, beta-blocker overdose,

     • Too tachy = not enough time to fill, decreased stroke volume

     • Too brady = decreased cardiac output, poor perfusion

   • Fluids must be carefully monitored or avoided to prevent further lung congestion. (the pump is broken…adding fluid will make the fluids collect in the lungs even moreso)

   • Diagnosed through signs such as hypotension, cool extremities, oliguria (low urine output), and wet lung sounds (crackles).

     • 50% mortality rate if all symptoms above present

   • Treatment = catheterization (i.e. get to the cath lab asap), o2 en route if they can tolerate, cardiovert for certain arrythmias, pacing with pads, certain medications such as amiodarone.

2. Obstructive Shock:

   • Obstruction impairs blood flow, typically involving conditions such as:

     • Cardiac Tamponade: Fluid accumulation around the heart, often presenting with Beck's triad: hypotension, JVD (jugular venous distension), and muffled heart sounds.

     • Tension Pneumothorax: Air in the pleural space compressing thoracic structures leading to acute hypotension.

     • Pulmonary Embolism (PE): Significant clots blocking blood flow to the lungs. Commonly causes dyspnea, chest pain, cyanosis, and signs of right heart failure.

Management Strategies

• For Cardiogenic Shock:

  • Administer inotropes like dobutamine to strengthen heart contractions without increasing rate.

  • Oxygen therapy, fluid management, and addressing the underlying cause (like MI).

• For Obstructive Shock:

  • Immediate recognition and treatment of cardiac tamponade or tension pneumothorax using thoracentesis or decompression.

  • PE management often initiates with oxygen and possibly anticoagulation therapy, depending on severity.

Peripheral Shock

• Addressed in terms of fluid loss and distribution abnormalities:

  • Hypovolemic Shock: Caused by blood loss or significant fluid depletion (e.g. severe vomiting, diarrhea).

  • Distributive Shock: Vessels lose tone, often due to septic, neurogenic, or anaphylactic shock. (Think: the pipe is too big to distribute the water needed to certain tissues in body)

Hypovolemic Shock

• Blood Loss Tolerance

  • Tolerance varies based on individual size and blood volume.

  • Stages of Hemorrhagic Shock:

    • Stage 1 (up to 15% blood loss, approx. 750 mL)

    • Stage 2 (15-30% blood loss, approx. 750-1500 mL)

    • Stage 3 (30-40% blood loss, approx. 1500-2000 mL)

    • Stage 4 (more than 40% blood loss, >2000 mL); leads to potential death.

Symptoms and Responses

• Vital Signs Changes:

  • Blood pressure typically maintained in early stages but drops significantly in stages 3 and 4.

  • Heart rate increases as compensation; bradycardia indicates severe shock progression.

  • Respiratory rate climbs as the body seeks oxygen due to low perfusion.

  • Urine output decreases due to reduced renal perfusion; Aldosterone response retains fluid, further decreasing urine.

Treatment Approaches

• Primary Goals:

  • Stop the bleeding.

  • Maintain oxygen delivery to tissues.

  • Prevent hypothermia.

• Methods to Stop Bleeding:

  • Direct pressure, tourniquets for extremity wounds, and occlusive dressings for neck injuries.

  • Consider pelvic binders for pelvic fractures; they compress the area to reduce blood loss.

  • Use of gauze and hemostatic agents in other regions where traditional pressure is difficult.

Trauma Triad of Death

• Consists of:

  • Hypothermia: Cold patients fail to clot. Can use blankets or warming devices.

  • Coagulopathy: Abnormal clotting can occur due to acidosis and hypothermia. Severity worsens with severe blood loss.

  • Acidosis: Increase in hydrogen ions leads to lower pH; can be buffered by bicarbonate.

Fluid Resuscitation

• Fluid Management:

  • Start with isotonic fluids; crystalloid is preferred for resuscitation.

  • Caution against fluid overload as it can exacerbate bleeding and acidosis.

• Fluid Boluses: Typically, 20 mL/kg is standard; in septic shock, may escalate to 30 mL/kg.

  • Target Mean Arterial Pressure (MAP) of at least 65 mmHg; higher (around 80 mmHg) if head injury is suspected.

Drug Therapies

• TXA (Tranexamic Acid):

  • Timely administration can help keep existing clots from breaking down.

  • Administered within the first 3 hours for best outcomes.

• Sepsis Considerations:

  • Major concern if two SIRS criteria are met: heart rate >90, respiratory rate >20, temperature abnormal, and abnormal white blood cell count.

Unique Cases of Shock

• Aortic Rupture: Can lead to hypovolemic shock; mortality very high if ruptured.

  • Differentiate between thoracic and abdominal aortic aneurysms based on symptoms.

  • Classic Symptoms:

    • Thoracic: differing blood pressures on arms.

    • Abdominal: pulsating mass.

Management of Neurogenic Shock

• Nerve Signals: Loss of sympathetic nervous system function leads to hypotension and warm, dry skin. (Remember: Neurogenic is also known as spinal shock. This shock typically involves an injury or a disconnect of the spinal cord, disabling the autonomic nervous systems, i.e. the body cannot tell itself to compensate like it should)

• Treatment: Administer fluids and catecholamines to help restore circulation and blood pressure.

Anaphylactic Shock

• Mechanics: Caused by widespread histamine release leading to vasodilation and low blood pressure.

• Recognizing Anaphylaxis: Requires involvement of multiple body systems (respiratory, circulatory, GI) with symptoms like urticaria, difficulty breathing, and hypotension.

• Intervention: Administer epinephrine, remove allergen, and consider adjunct meds like antihistamines or corticosteroids.

Key Takeaways

• Keep the patient warm and stop any ongoing bleeding.

• Monitor vital signs and adjust treatment based on response.

• Clear guidelines on managing fluid resuscitation to avoid overwhelming the patient.