The most important key to the pathophysiology

SEPTIC SHOCK

HYPOVOLEMIC SHOCK

ETIOLOGY

Sepsis is a systemic response to infection.

Manifested by two or more of the Systemic Inflammatory Response Syndrome criteria as a consequence of documented or presumed infection

Caused by hospital-acquired gram-negative bacilli or gram-positive cocci

Often occurs in immunocompromised patients and patients with chronic and debilitating diseases.

Rarely caused by Candida or other fungi

Postoperative infection should be suspected as the cause of septic shock in patients who have recently had surgery.

Uncommon form of shock caused by staphylococcal and streptococcal toxins is called toxic shock syndrome.

One of the most common cardiac complications.

Reduced intravascular blood volume causes circulatory dysfunction and inadequate tissue perfusion.

Vascular fluid volume loss causes extreme tissue hypoperfusion.

Internal fluid losses can result from hemorrhage or third-space fluid shifting.

External fluid loss can result from severe bleeding or from severe diarrhea, diuresis, or vomiting.

Inadequate vascular volume leads to decreased venous return and cardiac output.

PATHOPHYSIOLOGY

Microorganisms invade the body tissues an exhibit an immune response.

Immune response provokes the activation of biochemical cytokines and mediators associated with an inflammatory response.

Increase in capillary permeability and vasodilation interrupt the body’s ability to provide adequate perfusion, oxygen, and nutrients to the tissues and cells.

Proinflammatory and anti-inflammatory cytokines released during the inflammatory response and activates the coagulation system that forms clots whether or not there is bleeding occurring.

Imbalance of the inflammatory response and the clotting and fibrinolysis cascades are critical elements of the physiologic progression of sepsis in affected patients.

Fluid loss occurs either be internal or external fluid loss.

Results in a drop in arterial blood pressure activates the body’s compensatory mechanisms in an attempt to increase the body’s intravascular volume.

Diminished venous return occurs as a result of the decrease in arterial blood pressure.

Preload becomes reduced.

Stroke volume is decreased.

Cardiac output is decreased because of the decrease in stroke volume.

Reduced mean arterial pressure follows as the cardiac output gradually decreases.

Delivery of nutrients and oxygen to the cells are decreased.

Ultimately lead to multiple organ dysfunction syndrome

IMPORTANT PHYSICAL ASSESSMENTS

Assess if the patient has positive blood culture, currently receiving antibiotics, had an examination or chest x-ray, or has a suspected infected wound.

Assess for presence of hypotension, tachypnea, tachycardia, decreased urine output, clotting disorder, and hepatic abnormalities.

Hypotension

Decreased sensorium.

Tachycardia.

Rapid, shallow respirations.

Decreased urine output of less than 25ml/hour.

Cool, clammy, and pale skin.

Decreased blood pH, partial pressure of oxygen, and increased partial pressure of carbon dioxide.

Elevated potassium, serum lactate, and blood urea nitrogen levels.

NON-PHARMACOLOGICAL INTERVENTIONS

Oxygen support

Monitor hemodynamic status, fluid intake and output, and nutritional status.

Monitor CVP, PAOP, or ScvO_2, pulse oximetry, ABGs, blood glucose, lactate, and electrolyte levels, renal function

Monitor vital signs

Monitor weight

Oxygen administration

Treat underlying cause of fluid loss

Pneumatic anti shock garment

Modified Trendelenburg position

PHARMACOLOGICAL INTERVENTIONS

Perfusion restored with IV fluids and sometimes vasopressors

Broad-spectrum antibiotics

Other supportive measures such as corticosteroids, insulin.

Vasoactive drugs.

Insulin

Desmopressin

Antidiarrheal drugs.

Antiemetics.

Normal saline, Lactated Ringers, plasma expanders, plasma proteins