Different Types of Shock

Hypovolemic Shock Mechanism: Decreased Blood Volume: Leads to reduced filling of the ventricles, resulting in a decreased cardiac output (CO) and cardiac index. Baroreceptor Response: The decreased blood volume and cardiac output trigger the baroreceptors, leading to the narrowing of pulse pressure and a drop in systolic blood pressure (SBP) and mean arterial pressure (MAP). Cardiac Index Formula: Cardiac Index = Cardiac Output Body Surface Area Cardiac Index= Body Surface Area Cardiac Output ​ Example: For a cardiac output of 5 L/min and a body surface area (BSA) of 1.7 m², the cardiac index would be approximately 3 L/min/m². Compensatory Mechanisms: Sympathetic Activation: The body responds by increasing heart rate (↑ HR) and systemic vascular resistance to maintain blood pressure and perfusion to vital organs. Key Points: No Blockage of Sympathetic System: As there is no blockage, the sympathetic nervous system is activated, leading to increased heart rate and vascular resistance. Narrowed Pulse Pressure: This is a hallmark sign of hypovolemic shock, indicating a significant drop in blood volume and pressure. Types of Shock and Their Mechanisms 1. General Pathophysiology of Shock: Oxygen (O₂) Delivery to Tissue: Decreased O₂ delivery to tissues leads to lactic acid accumulation. Blood volume decreases, causing a reduction in central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP). Mean Arterial Pressure (MAP): When MAP falls below 60-65 mmHg, it leads to shock. 2. Cardiogenic Shock: Mechanism: Decreased Cardiac Output (CO): Caused by reduced myocardial contractility. Consequences: Leads to decreased systolic blood pressure (SBP), MAP (<65 mmHg), and narrowed pulse pressure. Signs: Increased jugular venous pressure (JVP) Increased right atrial pressure (RAP) Edema Increased PCWP Causes: Myocardial infarction (MI) Myocarditis Pressure overload Volume overload 3. Distributive Shock: Mechanism: Decreased Afterload: Leads to peripheral vasodilation, causing an increased cardiac output (CO). Consequences: Blood stagnation in peripheral vessels reduces tissue perfusion (indicated by increased serum lactate) and decreases venous return, CVP, and PCWP. Cardiac Index: >4.4 L/min/m² Types: Septic Shock: Caused by severe infection and systemic inflammation. Neurogenic Shock: Due to neural damage, such as in spinal cord injuries. Anaphylactic Shock: Severe allergic reaction causing vasodilation. Dysautonomic Shock: Related to autonomic nervous system dysfunction. 4. Obstructive Shock: Mechanism: Caused by physical obstruction of the heart or great vessels, preventing normal cardiac output. Causes: Cardiac Tamponade: Accumulation of fluid in the pericardium that compresses the heart. Pericardial Effusion: Fluid build-up around the heart. Tension Pneumothorax: Air in the pleural space that compresses the heart. Tumor in Mediastinum: Mass that increases intrathoracic pressure, restricting cardiac filling. Decreased Preload and Its Effects Causes of Decreased Preload: Severe Coarctation of the Aorta: A narrowing of the aorta, leading to increased afterload, which ultimately reduces preload. Saddle Embolus: A large blood clot that blocks pulmonary arteries, also increasing afterload and reducing preload. Consequences: Decreased Cardiac Output (CO) Decreased Cardiac Index Decreased Mean Arterial Pressure (MAP) Increased Serum Lactate (S. Lactate): Indicates impaired tissue perfusion and anaerobic metabolism. Hemodynamic Changes: Increased Central Venous Pressure (CVP): Indicates increased venous pressure due to the backlog of blood. Increased Pulmonary Capillary Wedge Pressure (PCWP): Reflects increased pressure in the left side of the heart due to backup of blood, often associated with left ventricular failure or severe obstruction like a saddle embolus. Decreased Vascular Compliance: Caused by the increased afterload, leading to stiffer blood vessels and reduced ability to accommodate blood flow.