Μυστηριώδεις Συμβολισμοί

SHOCK

• Shock is a life-threatening condition of circulatory failure, causing insufficient oxygen delivery to meet cellular metabolic needs, producing cellular and tissue hypoxia.
• Defined as a state of cellular and tissue hypoxia due to reduced oxygen delivery, increased oxygen consumption, inadequate oxygen utilization, or a combination of these.
• Commonly occurs when there is circulatory failure, manifested as hypotension (reduced tissue perfusion), but can also present as hypertensive or normotensive.
• Initially reversible, but immediate recognition and treatment are crucial to prevent progression to irreversible organ dysfunction.
• "Undifferentiated shock" is when shock is identified, but the cause is unclear.

Relevant Physiology

• Cardiac output (CO) is calculated as stroke volume (SV) multiplied by heart rate (HR).
• Preload: Myocardial sarcomere length just before contraction.
• Afterload: Resistance to ventricular ejection.
• Contractility: Change in peak force at a given initial fibre length (end-diastolic volume).
• Factors that determine preload include intrathoracic pressure, atrial pressure, right atrial pressure, mean systemic filling pressure, total venous blood volume, resistance to venous return, venous vascular compliance.
• Factors that determine afterload include ventricular wall compliance, duration of ventricular diastole, wall thickness, relaxation properties of the muscle, end-systolic volume of the ventricle, arterial resistance, arterial compliance, inertia of the blood column.

Interpretation of O₂ER

• High O₂ER suggests inadequate oxygen delivery (e.g. hypoxic hypoxia, anemia, altered cardiac contractility) or increased oxygen consumption.
• Low O₂ER suggests increased oxygen delivery or decreased oxygen consumption (e.g. hyperoxia, hypothermia, sedation, starvation).

Clinical Diagnosis of Shock

• Neurologic: Altered mental status (agitation, bradypsychic, bradylalia, coma)
• Pulmonary: Tachypnea
• Cardiac: Hypotension (MAP < 65 mmHg or significant drop from baseline values), bradycardia, and tachycardia (>120 bpm is associated with profound bleeding in hemorrhagic shock)
• Renal: Low urine output (<0.5 mL/kg/h), shock index (HR/SBPs) > 0.8 suggests hemodynamic instability.
• Peripheral perfusion/temperature: Temperature is decreased in shock, warm peripheral skin temperature predicts septic shock, skin mottling, prolonged capillary refill time.

Types of Shock

• Cardiogenic: Pump problem (e.g., MI, cardiomyopathy, arrhythmias, valvular dysfunction)
• Obstructive: Pipes problem (e.g., tension pneumothorax, cardiac tamponade, pericardial effusion, pulmonary embolism)
• Distributive: Tank problem (e.g., sepsis, anaphylaxis, neurogenic, septic)
• Hypovolemic: Tank problem (e.g., hemorrhage)

Cardiogenic Shock

• Represents the sequence of circulatory failure, hypoperfusion, and end-organ dysfunction caused by cardiac disease.
• SCAI Shock Classification categorizes shock stages (A-E) based on clinical presentation, hemodynamics, and need for support.
• Phenotypes & Severity: Different patterns of ventricular function, filling pressures, peripheral vascular tone, and congestion.
• The end-stage of cardiogenic shock is characterized by severe lactic acidosis, RV congestion, greater shock severity, and multiple organ failure.

Cardiogenic Shock - Monitoring

• Basic monitoring includes clinical examination, ECG, pulse oximetry, blood pressure, urine output, labs (u/cre, liver function tests, lactate).

Cardiogenic Shock - Management

• Treat the underlying etiology
• Respiratory stabilization (e.g., oxygen supplementation, mechanical ventilation)
• Hemodynamic stabilization (e.g., inotropic and vasopressor agents to optimise MAP)

Obstructive Shock - Cardiac Tamponade

• Pathophysiology: Compression of cardiac chambers due to increased pericardial pressure exceeding cardiac filling (diastolic pressures).
• Causes: Idiopathic (viral or immune-mediated), infectious (viral, bacterial, fungal, parasitic), noninfectious (autoimmune, neoplasm, cardiac, trauma), drug-induced, metabolic, radiation.
• Diagnosis: Tachycardia, hypotension, elevated jugular venous pressure (Kussmaul sign), pulsus paradoxus, echocardiography (pericardial effusion, chamber collapse).
• Management: Urgent pericardial fluid drainage (percutaneous pericardiocentesis or surgical approach).

Obstructive Shock - Pulmonary Embolism

• Pathophysiology: Increased RV afterload, RV dilation, TV insufficiency, RV wall tension, neurohormonal activation, myocardial inflammation, RV O₂ demand, Intrapulmonary A-V shunting, RV ischaemia, hypoxic injury.
• Echocardiography: Enlarged right ventricle, Dilated RV, Flattened intraventricular septum; Distended inferior vena cava with diminished respiratory collapsibility, tissue Doppler imaging.
• CT scan: Multifocal pulmonary emboli.
• Management: Anticoagulation, thrombolytic therapy, surgical pulmonary embolectomy, catheter-directed treatment.

Distributive Shock- Septic Shock

• Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection.
• Septic shock is a subset of sepsis, with underlying circulatory, cellular, and metabolic abnormalities contributing to a higher mortality risk than sepsis alone.
• Sepsis: Suspected/documented infection plus SOFA score >2. Septic Shock: Sepsis + vasopressor requirement to maintain MAP ≥ 65 mmHg and blood lactate > 2 mmol/L, absent hypovolemia.
• Defining characteristics include SOFA scores, presence of infection, vasopressor use, lactate levels.
• Management: Fluid resuscitation, vasopressors, and antimicrobial therapy.

Anaphylactic Shock

• Characterized by profound reduction in venous tone, hypovolemic shock features, fluid extravasation, and depressed myocardial function.
• Causes: Due to known or highly probable allergens.
• Pathophysiology: Myocardial ischemia, conduction defects, stress cardiomyopathy. Respiratory effects include upper airway symptoms (sneezing, rhinorrhea, dysphonia, laryngeal edema, laryngeal obstruction, oropharyngeal angioedema), and lower airway manifestations (cough, wheeze, pulmonary hyperinflation, edema, hemorrhage, respiratory failure, respiratory arrest.).
• Management: Rapid administration of epinephrine, normal saline bolus, oxygenation, and intubation.

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