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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 ScvO2, 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

Rosalind,

I thoroughly enjoyed reading your discussion post this week regarding shock. You made several excellent points and I found your post very informative! One point that stuck out to me the most was the statement you made that “the most important key to the pathophysiology and the type of diagnosed shock is the etiology”. The concept map that find found and posted is an excellent resource that can be used for students and even in the clinical setting such as a medical surgical floor. The several types of shock can be a difficult subject for students to understand learning tools such has the concept map you have found are an excellent learning tool.

Maisie


Great work on your chart in the Canvas discussion area. What are your plans for using charts in the teaching learning process with your future students (rather it be theory, lab or clinical)?

Dr. Cheryl,

Thank you for your feedback regarding my discussion post. I find visual tools such as charts are a helpful tool in aiding students in understanding complex subjects such as shock. I feel visual tools can be used in the learning process in the theory, lab, and clinical setting. In the theory setting is usually when a concept is first introduced therefore visual tools can help students grasp difficult concepts. In the lab setting procedures are usually learned and visual tools can be used to breakdown the steps in order to perform a procedure following protocol. Lastly charts such as the shock comparison chart I complied can be a useful tool in the clinical setting when assessing patients and developing care plans for patients suffering from either septic or hypovolemic shock.

Maisie


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