Shock and how to manage

Shock and how to manage

Shock is a life-threatening condition that occurs when the body's organs and tissues do not receive enough oxygen and nutrients due to low blood pressure. Shock can be caused by various factors, such as blood loss, infection, heart failure, allergic reaction, or trauma.


It can lead to multiple organ dysfunction syndrome (MODS), which is a major cause of death in intensive care units (ICUs). Therefore, it is crucial to recognize and treat shock promptly and effectively in ICU patients.

Pathophysiology of each type of shock

The pathophysiology of each type of shock is different and complex, but the final common pathway is poor perfusion, anaerobic metabolism, lactic acidosis, and mediator release with perpetual tissue damage1. Here is a brief summary of the pathophysiology of each type of shock:


  • Hypovolaemic shock: This type of shock occurs when there is a loss of intravascular volume from bleeding, vomiting, diarrhoea, or burns. This leads to a decrease in preload, stroke volume, cardiac output, and blood pressure. The body tries to compensate by increasing the heart rate, systemic vascular resistance, and venous return. However, if the volume loss is severe or prolonged, the compensatory mechanisms fail and tissue hypoperfusion ensues.


  • Cardiogenic shock: This type of shock occurs when there is a failure of the heart to pump blood effectively due to myocardial infarction, arrhythmia, cardiomyopathy, or valvular disease. This leads to a decrease in stroke volume, cardiac output, and blood pressure. The body tries to compensate by increasing the heart rate, systemic vascular resistance, and venous return. However, this also increases the myocardial oxygen demand and worsens the ischaemia and dysfunction of the heart. In addition, the reduced cardiac output causes pulmonary congestion and oedema, impairing gas exchange and oxygen delivery.


  • Distributive shock: This type of shock occurs when there is a widespread vasodilation due to sepsis, anaphylaxis, or neurogenic injury. This leads to a decrease in systemic vascular resistance, venous return, preload, stroke volume, cardiac output, and blood pressure. The body tries to compensate by increasing the heart rate and contractility. However, this may not be enough to overcome the profound vasodilation and hypotension. Moreover, in septic shock, there is also an imbalance between pro-inflammatory and anti-inflammatory mediators, causing endothelial dysfunction, microvascular thrombosis, increased capillary permeability, tissue oedema, organ damage, and impaired cellular metabolism.


  • Obstructive shock: This type of shock occurs when there is a mechanical obstruction of blood flow due to pulmonary embolism, cardiac tamponade, or tension pneumothorax. This leads to a decrease in venous return, preload, stroke volume, cardiac output, and blood pressure.

The body tries to compensate by increasing the heart rate and systemic vascular resistance.

However, this may not be enough to overcome the high afterload and reduced filling of the heart.

In addition, the obstruction causes increased pressure in the affected chamber or vessel, causing impaired ventricular function, right-to-left shunting, hypoxemia, and acidosis.

Management

To identify the type and cause of shock, there are four main types of shock: hypovolaemic, cardiogenic, distributive, and obstructive.

Each type has different causes, signs, and treatments. For example, hypovolaemic shock is caused by fluid loss from bleeding, vomiting, diarrhoea, or burns; cardiogenic shock is caused by impaired heart function from myocardial infarction, arrhythmia, or cardiomyopathy; distributive shock is caused by vasodilation from sepsis, anaphylaxis, or neurogenic injury; and obstructive shock is caused by mechanical obstruction of blood flow from pulmonary embolism, cardiac tamponade, or tension pneumothorax.


Assess the hemodynamic status of the patient, this includes measuring the vital signs (blood pressure, heart rate, respiratory rate, temperature), urine output, mental status, and peripheral perfusion (skin colour, temperature, capillary refill). In addition, invasive monitoring devices such as arterial catheters, central venous catheters, pulmonary artery catheters, or echocardiography may be used to measure more specific parameters such as arterial blood gas (ABG), central venous pressure (CVP), pulmonary artery pressure (PAP), cardiac output (CO), and mixed venous oxygen saturation (SvO2).


Initiate resuscitation and stabilization: the main goal of resuscitation is to restore adequate tissue perfusion and oxygen delivery by correcting the underlying cause of shock and supporting the vital organs. This may involve the following interventions:


  • Fluid therapy: Fluids are given intravenously to increase the intravascular volume and improve the preload and cardiac output. The type and amount of fluids depend on the type of shock and the patient's fluid status. Crystalloids (such as normal saline or lactated Ringer's solution) are preferred over colloids (such as albumin or hydroxy ethyl starch) for most types of shock. Fluid responsiveness can be assessed by using dynamic indices such as pulse pressure variation (PPV) or stroke volume variation (SVV), which reflect the changes in arterial pressure or stroke volume in response to mechanical ventilation.


  • Vasopressors: Vasopressors are drugs that constrict the blood vessels and increase the systemic vascular resistance and blood pressure. They are used when fluids alone are not sufficient to maintain a mean arterial pressure (MAP) above 65 mmHg or when fluids are contraindicated due to pulmonary oedema or cardiac failure. The choice of vasopressor depends on the type of shock and the patient's hemodynamic profile. The most commonly used vasopressors are norepinephrine (first-line agent for most types of shock), epinephrine (second-line agent for septic shock or anaphylactic shock), dopamine (third-line agent for cardiogenic shock or bradycardia), phenylephrine (alternative agent for neurogenic shock or tachyarrhythmia), and vasopressin (adjunctive agent for refractory septic shock).


  • Inotropes: are drugs that increase the contractility and stroke volume of the heart. They are used when there is evidence of myocardial dysfunction or low cardiac output despite adequate fluid resuscitation and vasopressor support. The most commonly used inotropes are dobutamine (first-line agent for cardiogenic shock or septic shock with low CO), milrinone (second-line agent for cardiogenic shock with high SVR), and levosimendan (alternative agent for cardiogenic shock with low CO).


  • Oxygen therapy: is administered via nasal cannula, face mask, or mechanical ventilation to maintain a pulse oximetry (SpO2) above 94% or an arterial oxygen saturation (SaO2) above 90%. Oxygen therapy should be titrated to avoid hyperoxia or hypoxia, which can both worsen tissue injury and organ dysfunction.


  • Other specific therapies: Depending on the type and cause of shock, other specific therapies may be indicated


Source: 4/3/2023(1) Pathophysiology of Shock - ScienceDirect. https://www.sciencedirect.com/science/article/abs/pii/S0899588518308165 Accessed 4/3/2023.

(2) Definition, classification, aetiology, and pathophysiology of shock in .... https://www.uptodate.com/contents/definition-classification-etiology-and-pathophysiology-of-shock-in-adults Accessed 4/3/2023.

(3) Pathophysiology of shock - PubMed. https://pubmed.ncbi.nlm.nih.gov/2192723/ Accessed 4/3/2023.

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