Septs and Septic shock

1. Introduction to Shock

Shock is a state of cellular and tissue hypoxia due to reduced oxygen delivery, increased oxygen consumption, inadequate oxygen utilization, or a combination of these processes. It is a life-threatening condition where the body's metabolic demands exceed the supply.

Pathophysiology of circukatory system

  • Cardiolovascular system unable to deliver adequate oxygen to tissues

  • Cellular dysfunction and shift to anaerobic metabolism

  • incrase blood lactate concentration

  • cellular, tissue, and organ dysfunction

  • Multi-organ dysfunction; death

Pathophysiology of Circulatory shock

Determinats of tissue oxygenation

    oxygen delivery: determined by cardiac output, hemoglobin levels, and arterial oxygen saturation, which collectively influence the amount of oxygen reaching tissues.

Compensation:

  • Vasoconstriction

  • MAP appears adequat but ox

  • ygen delivery is inadequate .

Clinical presentation:

  • Altered vital signs:

    • decreased MAP and/or SBP, tachycardia, tachypenea

    • Organ dysfunction: Brain

      • Altered mental status, confusion, or decreased responsiveness.

    • Kidneys: AKI

    • Lungs: decreased oxygen daturation (<94%)

    • Heart: altered hemodynamics

  • Mean Arterial Pressure (MAP): The average pressure in a patient's arteries during one cardiac cycle. It is considered a better indicator of perfusion to vital organs than systolic blood pressure.

    • MAP=23DBP+13SBPMAP=\frac23DBP+\frac13SBP

    • Goal MAP is typically ≥65 mmHg\ge 65 \text{ mmHg} in most shock states.

  • Cardiac Output (CO): The volume of blood pumped by the heart per minute.

    • CO=HR×SVCO = HR \times SV

  • Systemic Vascular Resistance (SVR): The resistance offered by the peripheral circulation.

2. Classification of Shock

Shock is generally categorized into four main types based on the underlying physiological mechanism:

  1. Hypovolemic Shock

    • Caused by circulatory failure due to extracellular volume depletion leads to decreased preload. This type of shock can result from significant blood loss, dehydration, or severe burns, ultimately impairing the body's ability to maintain adequate organ perfusion.

    • Characteristics: low preload, low CO, High Afterload

  2. Cardiogenic Shock (less common)

  • Caused by pump failure (e.g., Myocardial Infarction, arrhythmias, heart failure).

  • Characteristics: high preload, low CO, High afterload

  • Symptoms/signs: hypotension, low CO, Organ failure, related to causes

3. Vasoilatory Shock

  • Caused by excessive vasodilation and impaired distribution of blood flow.

  • Includes Sepsis (most common), anaphylaxis (sever systemic allergy), and neurogenic shock (including spinal cord injury).

  • Characteristics: High CO (early/warm phase), low SVR, low/normal PCWP.

  1. Obstructive Shock

  • Caused by physical obstruction t

  • o blood flow (e.g., Pulmonary Embolism, cardiac tamponade).

  • Characteristics: High preload, Low CO, High afterload

3. Sepsis and Septic Shock

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection.

3.1 Sepsis-3 Definitions

  • Sepsis: Organ dysfunction is identified as an acute change in total Sequential Organ Failure Assessment (SOFA) score ≥2\ge 2 points consequent to the infection.

    • Documented or probable infection

    • 2 or more systemic inflammatory response syndrome (SIRS) criteria:

      • Temperature >38 C or < 36 C

      • HR > 90

      • RR > 20

      • WBC > 12000 or < 4000 or > 10% bands

  • Septic Shock: Sepisis with persisting hypotension (MAP < 65) and ALL 3 of these criterias:

    • Reuiring vasopressor use

    • Having a serum lactate level >2 mmol/l

    • Dispite having received adequate volume resusciation

      • 30 ml/kg crystalloid fluids

  • Associated with increasing mortality compared to sepsis

  • Risk factors for infection

    • extremes of age

    • presence of pre-existing conditions

      • HF, diabetes, COPD, Cirrhosis, Alcohol dependence, End stage renal disease , cancer, HIV

  • Cites of infection

    • Lungs, intra-abdominal space, genitouriary tract (no bloodstreme)

  • Pathogens

Gram-negative bactera

  • E.Coli

  • Klebsiella

  • Proteus species

  • Enterobacter species

  • Pseudomonas aerugionsa (high mortality rate)

Gram-positive bacteria

  • Staphylococcus aureus

  • CONS

  • Enterococcus species

  • Streptococci pneumoniae

Why does infection become sepsis/

  • cellular components for initiating inflammation

    • Gram-negative spesis

      • Endotoxin component of gram-negative cell wall

        • Lipid A component is highly immunoreactive

        • Triggers macrophage activation and inflammatory cascades

    • Gram-positive sepsis

      • Peptidoglycan on cell wall surface

        • Pro-inflammatory

        • Less potent than endotoxins

  • Pro and anti inflammatory medicators

    • Relesed by endothelial cells and macrophages

    • act locally

    • work simultaneously

    • attempt to eradicate infection without harming host

    • Pro inflammatory response

      • Attempt to eliminate invading pathogens

      • damage host tissue

      • TNF-alpha, IL-6, IL 12 released by enothelial cells and macrophages

    • Anti-inflammatory responses

      • Limit local and systemic tissue injury

      • active leukocytes

      • IL-1 receptor antagonist, IL-4, IL 10

    • Systemic inflammation causes:

      • Injured endothelial cells

      • decreased arteriolar responsiveness to vasodilators and vasoconstrictiors

      • decreased blood flow into capillaries

      • neutrophil infiltration and protein leakage into venules

  • Coagulation cascade

    • pro-inflammatory cytokines cause hypercoagulable state

      • Through pro-coagulant and anti-fibrinolytic mechanisms

      • thrombin continues to form

    • Anti-inflammatory medicators lead to depression of fibrinolytic activity, resulting in enhanced clot stability and prolonged thrombus formation.

    • overall result: hypercoagulatable state

Complication of sepsis

  • Organ damage due to tissue damage and hypoperfusion

    • Kidney, lung, heart

  • Septic shock

  • Disseminated intravascular coagulation (DIC): a serious complication that can arise in septic shock, leading to widespread clotting in small blood vessels, further exacerbating organ damage and contributing to multiple organ failure.

  • Hemodynamic effect: hypotension, tachycardia, high CO, mydocardial dysfunction, dysregulation of vasculature

  • End result: organ hypoperfusion

Clinical presentation

  • Varies widely depending on:

    • Site of infection

    • Balance of pro-and anti-inflammatory response

    • Host factors

  • Early sepsis (first 6 hours)

    • General malaise or myalgia

    • Non-specific signs:

      • Fever or hypothermia

      • Elevated WBC

      • Chills

      • Tachycardia

      • Tachypnea

      • Change in mental status

  • Late sepsis

    • Depend upon the site of infection and organ dysfuction

      • Hypothension leading to organ dysfunction

      • Oliguria

      • Hypo or hyperventilation

      • Hyperlactemia

      • Hypo or Hyperglycemia

      • Leukopenia or leukocytosis; fever; additional evidence of infection

      • Continued or worsened decreases in mental status