emergency med lec 2 Comprehensive Clinical Guide to Shock and Hemorrhagic Management

Procedural Skills and Hands-on Learning Objectives

• Future Physical and Technical Training: The speaker emphasizes moving beyond textbook and slide-based learning to provide hands-on experience in the emergency department.

• Specific Skills to be Covered:     * Airway Management: Practice with jaw thrusts, using a laryngoscope, and the glidescope to observe the glottis.     * Procedures: Performing a drug push and other device applications.

• Practical Application: The goal is to bring mannequins and equipment to ensure providers move beyond theoretical knowledge to physical proficiency.

Definition and Pathophysiology of Shock

• Definition: Shock is defined as evidence of inadequate organ hypoperfusion.

• Etiology: It occurs when blood flow is insufficient to supply the basic metabolic needs of internal organs.

• Core Consequences:     * Hypoxia: A supply issue where organ tissues do not receive enough oxygen.     * Waste Removal: A failure to remove waste products of metabolism, contributing to a toxic state.

• Shift in Metabolism:     * Aerobic to Anaerobic Transition: When demand exceeds supply, cells shift to anaerobic metabolism.     * Lactic Acid Production: This shift creates lactic acid, leading to metabolic acidosis.     * Ischemia: Ischemia can occur in the heart, brain, and kidneys. If caught early at the lactate level, the outcome is improved; if it progresses to cellular breakdown and necrosis, it leads to widespread organ failure and death.

Biomarkers and Electrolyte Disturbances

• Lactate Levels: Often measured via a VBG (Venous Blood Gas). An elevated lactate level indicates inadequate perfusion.

• Potassium ($K^+$) Dynamics:     * Normal Location: $96\%-98\%$ of the body's potassium is located intracellularly.     * Normal Blood Levels: Typically range from $3.5$ to $4.4$ in a basic metabolic test.     * Hyperkalemia in Shock: Cellular necrosis causes potassium to leak out of cells, leading to high blood potassium levels.

• Cardiac Consequences of Hyperkalemia:     * EKG Progression:         1. Peaked T-waves: T-waves become larger and potentially taller than the QRS complex.         2. Disappearing T-waves: As levels rise, the T-wave morphology degrades.         3. Widened QRS: The QRS complex broadens significantly.         4. Sine Wave: A pre-morbid state where the QRS and T-wave fuse into a sine waveform, indicating imminent cardiac arrest.

• At-Risk Populations: Patients with renal failure are the number one group at risk for hyperkalemic complications.

• Phosphates: Critical component of ATP (Adenosine Triphosphate). Without ATP, muscle and heart function fails.

Cardiogenic and Obstructive Shock

• Cardiogenic Shock (Pump Failure):     * Acute Myocardial Infarction (AMI): The most common cause.     * Widowmaker: An occlusion of the LAD (Left Anterior Descending) artery, which supplies two-thirds of the myocardium and the septum.     * EKG Indicators: ST-segment elevations in leads $V_1, V_2, V_3, V_4$ (Anterior/Septal) and potentially $V_5, V_6, I, L$ (Lateral).     * Valve Failure: Acute mitral valve insufficiency presents as a loud systolic murmur and pulmonary rales/crackles.     * Myocardial Contusion: The heart can become "stunned," akinesis (lack of movement), or dyskinesis (bulging) following blunt chest trauma (e.g., slamming into a dashboard without a seatbelt).

• Cardiac Tamponade:     * Beck’s Triad: Hypotension, jugular venous distension (neck veins like "two ropes"), and muffled (distant) heart sounds.     * Pathophysiology: Fluid in the pericardium compresses the heart, preventing adequate filling (preload issue).     * Electrical Alternans: An EKG finding where QRS complexes alternate between large and small sizes as the heart "sloshes" in the pericardial fluid.     * Treatment: Pericardiocentesis or surgical intervention.

• Tension Pneumothorax:     * Clinical Signs: Hyper-resonance on percussion, decreased/absent breath sounds, and tracheal deviation away from the affected side.     * Pathophysiology: Air pressure kinks the vena cava, preventing venous return (preload issue).     * Diagnosis: Must be clinical, not radiological. Waiting for an X-ray can result in patient death.     * Treatment: Needle decompression (second intercostal space, above the third rib) followed by a chest tube at $20\,cm$ negative pressure.

Neurogenic Shock

• Definition: The hemodynamic consequence of high spinal cord injury (cervical or high thoracic).

• Mechanism: Destruction of sympathetic fibers leading to massive vasodilation (increased venous capacity).

• Presentation:     * Skin: Warm and dry (unlike hemorrhagic shock).     * Heart Rate: Low or normal (loss of fight-or-flight response).     * Neurology: Evidence of paralysis (paraplegia or quadriplegia).

• Management:     * "Fill the Tank": Aggressive fluid resuscitation is the first step toward filling the expanded venous space.     * Vasoconstrictors: Used only if fluids fail. Starting with vasoconstrictors (e.g., Norepinephrine, Dopamine) before filling the tank increases mortality due to tissue ischemia.

Classification of Hemorrhagic Shock

• Irreversible Shock: Threshold usually crossed at $30\%-50\%$ blood volume loss. At this point, stopping the bleed and replacing factors/platelets may not prevent death due to systemic damage.

• Class I Shock (Minimal Loss):     * Volume Loss: Up to $15\%$ (approx. < 800\,ml).     * Symptoms: Heart rate < 100\,bpm, respiratory rate < 20\,bpm, normal blood pressure, slightly anxious.     * Management: May not require IV fluids if bleeding is controlled.

• Class II Shock (Mild Loss):     * Volume Loss: $15\%-30\%$ (approx. $800\,ml - 1.5\,L$).     * Symptoms: Heart rate > 100\,bpm, tachypnea ($20-30\,bpm$), pulse pressure narrows, skin cool.     * Management: Fluids usually sufficient; blood might be needed if pre-existing anemia exists.

• Class III Shock (Moderate Loss):     * Volume Loss: $30\%-40\%$ (approx. $1.5\,L - 2\,L$).     * Symptoms: Hypotension (Systolic drops), significant tachycardia/tachypnea, mental status changes (distractibility, impending doom), low urine output.     * Management: Requires blood and fluids.

• Class IV Shock (Severe Loss):     * Volume Loss: > 40\% (approx. > 2\,L).     * Symptoms: Comatose/lethargic, negligible urine output, crashing blood pressure.     * Management: Immediate transfusion and surgical intervention.

Treatment and Management of Hemorrhage

• Primary Steps: Direct pressure first. Elevate the limb and use pressure points if necessary.

• Tourniquets:     * CAT (Combat Application Tourniquet): Designed for rapid self-application. It must be cranked tight enough to occlude arterial flow (it will be painful).     * Caveat: Re-evaluate every $8-10$ minutes to check if it can be loosened, but do not risk excessive re-bleeding.

• Digital Control: Using a gloved finger to directly plug a spurting vessel (e.g., axilla, neck, joints).

• Volume Resuscitation:     * Universal Donor: O-negative blood is used for those with unknown types. O-positive can be given to men or non-childbearing women to preserve O-negative stocks ($80\%-90\%$ of the population is Rh positive).     * Coagulopathy Warning: Giving only red cells dilutes clotting factors, leading to DIC (Disseminated Intravascular Coagulopathy). If more than $3-4$ units of blood are given, provide FFP (Fresh Frozen Plasma) and platelets.

Diagnostic Caveats and Special Populations

• Respiratory Rate: Often poorly measured; clinicians sometimes guess $16-20$ instead of counting. Normal adult rate is $12-16$ or $18$; $20$ is for a child.

• Urine Output: A gold standard for monitoring perfusion. Normal is $0.5$ to $1\,ml/kg/hr$ ($40-60\,cc/hr$ for an $80\,kg$ adult).

• The Elderly: May present with a feeling of "impending doom." Do not dismiss altered mental status as just "psychiatric" or "intoxication"; investigate metabolic causes.

• Pregnancy:     * Maternal blood volume is increased, which can delay shock signs.     * Aortocaval Compression: A pregnant uterus in the 2nd/3rd trimester can compress the inferior vena cava when the patient is supine.     * Positioning: Always place pregnant patients in the left lateral decubitus position or manually displace the uterus to ensure preload.

• Athletes: May have a baseline heart rate of $35-38\,bpm$. A heart rate of $90\,bpm$ in an elite athlete might represent significant shock.

• Medicated Patients: Those on Beta-blockers or Calcium Channel Blockers, or those with pacemakers, may not develop tachycardia despite severe shock.

Questions & Discussion

• Q: How do you distinguish localized vs. generalized hypoperfusion?     * A: A clot (arterial occlusion) causes localized coolness; generalized shock causes coolness throughout the entire body.

• Q: Does tracheal deviation occur in Cardiac Tamponade?     * A: No, tracheal deviation is specific to Tension Pneumothorax due to the pressure buildup in the thoracic cavity.

• Q: How sterile must needle decompression be?     * A: While a Betadine swipe is preferred, in a life-saving street emergency, the priority is decompression. Skin acts as a barrier; infection risk is low compared to the risk of death from the tension.

• Q: What do leads V5 and V6 indicate?     * A: Leads $V_5, V_6, I,$ and $L$ represent the lateral aspect of the heart.

• Q: What would a posterior MI show?     * A: It would typically show reciprocal ST-segment depressions in leads $V_1$ and $V_2$. Posterior leads placed on the back would show elevations.