shock

Shock, SIRS, Sepsis, and Multiple Organ Dysfunction Syndrome (MODS)

Shock

  • Definition: A syndrome characterized by decreased tissue perfusion and impaired cellular metabolism.

  • Mechanism: The imbalance between the supply of and demand for O2 and nutrients; hypoperfusion causes demand to exceed supply at the microcirculatory level, leading to ischemia, which results in cell injury and death.

  • Pediatric Treatment: Involves fluid resuscitation and frequent reassessment.

  • Most common cause of shock: Dehydration.

Classification of Shock

  • Main Categories: Four main categories of shock exist:

    • Cardiogenic Shock

    • Hypovolemic Shock

    • Absolute

    • Relative

    • Distributive Shock

    • Neurogenic

    • Anaphylactic

    • Septic

    • Obstructive Shock

  • Pathology: The cause, presentation, and management of shock vary per type, yet the physiological responses of cells to hypoperfusion are similar across categories.

Cardiogenic Shock

  • Definition: Results from systolic or diastolic dysfunction leading to decreased cardiac output (CO), stroke volume (SV), and blood pressure (BP).

  • Systolic Dysfunction: Inability of the heart to pump blood forward, compromising myocardial perfusion, affecting myocardial function, and ultimately decreasing CO.

  • Most common cause: Myocardial infarction (MI).

  • Key Factors impacting output:

    • Decreased filling of the heart leads to decreased stroke volume.

    • The left ventricle is primarily affected since systolic pressure is greater on the left side; lesser blood flow occurs through pulmonary circulation on the right side.

Precipitating Causes of Cardiogenic Shock

  • Myocardial infarction

  • Cardiomyopathy

  • Dysrhythmias

  • Blunt cardiac injury

  • Severe systemic or pulmonary hypertension

  • Cardiac tamponade

  • Myocardial depression from metabolic issues

  • Valvular disorders or structural heart issues, such as ventricular septal rupture.

Pathophysiology of Cardiogenic Shock

  • Primary Ventricular Ischemia:

    • Systolic Dysfunction: Results in ineffective forward movement of blood leading to lower stroke volume and cardiac output and reduced cellular oxygen supply and tissue perfusion.

    • Diastolic Dysfunction: Ineffective filling leads to increased pulmonary pressure, pulmonary edema, and impaired cellular metabolism.

  • Implications include decreased oxygenation and adverse effects on metabolism.

Manifestations of Cardiogenic Shock

  • Early Manifestations (Similar to acute heart failure):

    • Tachycardia, hypotension, narrowed pulse pressure, increased systemic vascular resistance (SVR), increased myocardial O2 consumption.

  • Physical Assessment Findings:

    • Tachypnea, pulmonary congestion, pallor, cool and clammy skin, decreased capillary refill time.

    • Neurological changes: anxiety, confusion, agitation due to poor cerebral perfusion.

    • Increased pulmonary artery wedge pressure (PAWP).

    • Decreased renal perfusion noted by reduced urinary output and sodium/water retention.

  • Diagnostic Studies:

    • Elevated lab values: BUN, PTT/PT INR, D-dimer, lactate, liver enzymes, hemoglobin, glucose.

    • Important consideration: Understand underlying reasons, not just memorize.

Progressive Cycles of Cardiogenic Shock

  • Involves cycles of inflammation, ischemia, vasoconstriction, and volume overload resulting from primary cardiac insult and myocardial dysfunction.

  • Consequences include hypoxemia, microcirculatory dysfunction, and systemic inflammatory response syndrome (SIRS) leading to potential multiorgan dysfunction and death.

  • Key metrics:

    • Systolic Blood Pressure < 90 mm Hg.

    • Cardiac Index < 2.2 l/min/m².

    • Cardiac Power Output < 0.6 W.

    • Lactic acidosis implicating potential organ perfusion issues.

Hypovolemic Shock

  • Absolute Hypovolemic Shock: Characterized by loss of intravascular fluid volume to support perfusion.

    • Common causes: hemorrhage, gastrointestinal loss (vomiting, diarrhea), fistula drainage, diabetes insipidus, diuresis.

  • Relative Hypovolemic Shock: Results from fluid relocating from vascular space to extravascular space (e.g., burns).

    • Known as 'third spacing'.

Pathophysiology of Hypovolemic Shock

  • Both absolute and relative hypovolemia lead to:

    • Decreased circulating volume

    • Decreased venous return

    • Decreased stroke volume

    • Decreased cardiac output

    • Insufficient cellular oxygen supply and tissue perfusion.

  • Impaired cellular metabolism ultimately ensues.

Response to Acute Volume Loss

  • Varies based on:

    • Extent of injury

    • Patient's age

    • Overall health status.

  • Compensatory Mechanisms:

    • Patient may compensate for up to 15% blood loss (approximately 750 mL); loss of 15-30% triggers sympathetic nervous system (SNS) response to increase heart rate, cardiac output, and respiratory rate, but decreases stroke volume.

    • Loss exceeding 30% leads to failure of compensatory mechanisms necessitating blood transfusions.

    • Loss of 40% total blood volume leads to tissue destruction.

Manifestations of Hypovolemic Shock

  • Anxiety, tachypnea, decreased urine output, and signs of renal failure.

  • Replacement of fluid is critical for reversal of damage.

  • Impact on vital signs: increased heart rate and respiratory rate while decreased stroke volume, central venous pressure (CVP), and pulmonary artery wedge pressure (PAWP).

Distributive Shock

  • Neurogenic Shock:

    • Occurs due to hemodynamic phenomena following spinal cord injury, particularly at the T5 vertebra or above.

    • Can last up to 6 weeks and is characterized by massive vasodilation without compensatory response from the SNS.

    • Pooling of blood occurs, leading to hypoperfusion and impaired cellular metabolism.

  • Clinical Manifestations:

    • Hypotension, bradycardia, inability to thermoregulate, dry skin, and poikilothermia (taking on the temperature of the environment).

Anaphylactic Shock

  • Life-threatening hypersensitivity reaction to an allergen.

  • Characterized by rapid massive vasodilation, release of vasoactive mediators, and increased capillary permeability leading to fluid leak into interstitial space, causing respiratory distress and circulatory failure.

  • Manifestations: Sudden onset including anxiety, confusion, chest pain, swelling of the lips/tongue, wheezing, stridor due to laryngeal edema, flushing, and pruritus.

Septic Shock

  • Defined as sepsis with hypotension unresponsive to fluid resuscitation and inadequate tissue perfusion leading to hypoxia.

  • Characterized by persistent hypotension and has a high mortality rate with various pathophysiologic effects involving both pro-inflammatory and anti-inflammatory responses.

  • Manifestations of Septic Shock:

    • Tachypnea/hyperventilation leading to respiratory alkalosis, potential respiratory failure (develops in ~85% of patients).

    • Altered neurological status, gastrointestinal dysfunction, diminished urine output.

Obstructive Shock

  • Occurs from physical obstructions to blood flow leading to decreased cardiac output.

  • Causes include cardiac tamponade, tension pneumothorax, or abdominal compartment syndrome.

  • Symptoms typically include Jugular Venous Distention (JVD) and pulsus paradoxus; rapid assessment is critical prior to cardiac arrest.

Stages of Shock

  • Shock is categorized into four overlapping stages:

    • Initial Stage: Often not clinically apparent; metabolism shifts from aerobic to anaerobic, leading to lactic acid accumulation.

    • Compensatory Stage: Drop in blood pressure and narrowed pulse pressure triggers SNS activation; clinical manifestations reflect body's attempts to maintain oxygen supply.

    • Impaired gastrointestinal motility, cool clammy skin (except for septic patients who may be warm and flushed).

    • Progressive Stage: Patient develops organ failure; aggressive treatment needed to prevent MODS (Multiple Organ Dysfunction Syndrome).

    • Refractory Stage: Multi-organ failure ensues; recovery is unlikely due to overwhelming waste accumulation and loss of compensatory mechanisms.

Diagnostic Studies

  • Complete patient history and physical assessment are crucial. No single study can diagnose shock.

  • Lab tests revealing elevated lactate and base deficit.

  • ECG monitoring, chest X-ray, continuous pulse oximetry, and hemodynamic monitoring are all essential facets of the diagnosis and management.

Interprofessional Care

  • Focus on optimizing oxygen delivery and supply, fluid replacement, using medications to support circulation, and addressing tissue oxygen demand.

  • Beware of complications from aggressive volume resuscitation, such as hypothermia and coagulopathy.

  • Ensure appropriate volume expansion in cases of septic, hypovolemic, and anaphylactic shock.

  • Nutritional Therapy: Start enteral nutrition promptly to minimize morbidity due to shock, aiming for a total energy expenditure increase of 1.5-2 times normal.

Pediatric Considerations

  • Unique aspects of pediatric treatment include different dosages, equipment, and psychological responses.

  • Specific attention to thermoregulation and fluid volume changes is essential due to higher metabolism and lower fluid reserves in children.

  • Common causes of pediatric shock encompass dehydration, trauma, sepsis, and anaphylaxis.

SIRS and MODS

  • Systemic Inflammatory Response Syndrome (SIRS): Defined by general inflammation across organs, often triggered by various insults like trauma, ischemia, or microbial factors.

  • Multiple Organ Dysfunction Syndrome (MODS): Refers to the failure of two or more organ systems due to SIRS, resulting in homeostatic instability requiring intervention.

  • Pathophysiology Implications: Includes release of inflammatory mediators, increased vascular permeability, organ dysfunction, and potential development of DIC (Disseminated Intravascular Coagulation).

  • Interprofessional care is focused on early detection and prevention of progression from SIRS to MODS, aggressive management of infection, maintenance of tissue oxygenation, and addressing metabolic needs to preserve organ function.