Sepsis and Shock Study Notes (Transcript-Based)

Section 1: Pre-shock and Shock Progression

• Core concept: perfusion and progression from pre-shock to shock to end-organ dysfunction; cells rely on adequate perfusion to deliver oxygen for aerobic metabolism. When perfusion falls, cells shift to anaerobic metabolism, lactic acid buildup, acidosis, and organ dysfunction.
• First clinical cue in shock progression: persistently decreasing urine output. In the lecture, the instructor notes that the very first sign of poor perfusion can be a urine output that falls below the critical threshold: ext{Urine output} < 30\frac{\text{mL}}{\text{kg} \cdot \text{hr}}. If at 30\ \frac{\text{mL}}{\text{kg} \cdot \text{hr}} you’re probably too late.
• Example scenario used in class: gunshot wound leading to bleeding and hypotension; review emphasizes recognizing the category of shock early for exam success.
• Distinction between deficits and excess: deficits (hypovolemia) vs excess (hypervolemia) discussed to frame nursing assessment and interventions. Dehydration is a cause of hypovolemia; excess fluid can lead to edema and caregiver vigilance about third spacing.
• Key nursing emphasis: not just memorizing signs, but understanding which type of shock is present and why. Links to cardiovascular effects (perfusion), renal perfusion (urine output), and cerebral perfusion (neurological status).

Section 2: Hypovolemic Shock and Fluid Balance

• Definition of hypovolemia as a deficiency of water without electrolyte deficiency.
• Common etiologies mentioned: dehydration, blood loss (e.g., gunshot wound), burns in emergent phase, vomiting and diarrhea causing fluid loss.
• Pathophysiology: reduced intravascular volume decreases venous return, cardiac output, and tissue perfusion; leads to compensatory mechanisms initially (tachycardia, vasoconstriction) and progress to organ dysfunction if not corrected.
• Third-spacing concept: shifts of fluid into interstitial spaces (third spaces) causing edema and tissue swelling; protective tissue wrapping advised for edema-prone areas; monitor for excess fluids as perfusion improves but edema worsens.
• Burn patient fluid dynamics: during emergent phase, marked hypovolemia; during acute phase, diuresis occurs and edema shifts and tissue perfusion change.
• Vital signs and monitoring cues:
  • Signs of poor perfusion: cold extremities, poor capillary refill, tachycardia, possible hypotension in progressing shock.
  • Orthostatic BP measurements (sitting, standing) to detect perfusion and autonomic response changes.
  • Weight monitoring and diuresis follow-up; weight loss reflects fluid loss; weight gain could indicate fluid overload.
• Nursing interventions for hypovolemia:
  • Fluid resuscitation with isotonic fluids (e.g., normal saline, lactated Ringer’s) to restore intravascular volume; bolus therapy when indicated.
  • Correct underlying causes (e.g., treat dehydration, control bleeding, manage vomiting/diarrhea).
  • Monitor and maintain urine output; target perfusion restoration while avoiding fluid overload.
  • Monitor skin integrity and edema; protect tissues at risk due to edema and third-spacing.
  • Reassess hemodynamics frequently (vital signs every few minutes if unstable).
• Hypokalemia in the context of hypovolemia: addressing dehydration and vomiting helps correct potassium deficit; IV fluids with appropriate electrolyte content and antiemetics may be used; avoid unnecessary fluid losses.
• Evaluation prompts: look for signs of hypovolemia vs other etiologies of shock; hypovolemia is usually associated with decreased blood pressure, tachycardia, tachypnea, and reduced urine output.

Section 3: Sepsis and Septic Shock – Pathophysiology and Management

• Definition: sepsis is a systemic response to infection; disseminated infection may lead to septic shock if untreated.
• At-risk population details mentioned:
  • Neutropenic patients (ANC < 500) due to bone marrow suppression (e.g., hematology/oncology context); fever with suspected infection in these patients triggers immediate actions.
  • Central lines (catheters) as a source of infection requiring careful monitoring and education on line care.
• Immediate management principles discussed:
  • In suspected sepsis, cultures should be drawn and broad-spectrum antibiotics started promptly, ideally within t \le 20\ \text{minutes} of patient arrival to ER, to reduce progression to septic shock and organ failure.
  • Common broad-spectrum antibiotics noted: Zosyn (piperacillin-tazobactam) and Meropenem. Zosyn contains a penicillin; caution in patients with penicillin allergy; Meropenem’s exact contents not specified in-table but noted as broad-spectrum.
  • Antibiotic choices aim to cover likely pathogens while awaiting cultures; reassess therapy based on culture results and allergy history.
• Severity and progression:
  • Sepsis can progress to septic shock, characterized by persistent hypotension and tissue hypoperfusion despite adequate fluid resuscitation in some cases; organ dysfunction can ensue (e.g., AMS, elevated lactate, DIC).
  • Laboratory cues include elevated lactic acid; elevated lactate correlates with tissue hypoperfusion and anaerobic metabolism.
• Hemodynamic and physiologic changes in septic shock (distributive shock):
  • Decreased systemic vascular resistance due to vasodilation; increased capillary permeability; plasma proteins leak into interstitium reducing intravascular volume.
  • Cardiac output may fall due to decreased preload and maldistributed volume, leading to reduced tissue perfusion and urine output.
  • Potential signs: hypotension, reduced urine output, altered mental status (acute encephalopathy), coagulation abnormalities like DIC, fever or hypothermia, and elevated lactate.
• Diagnostics and monitoring:
  • Frequent vital signs and continuous monitoring; monitor level of consciousness, vital signs, and urinary output.
  • Lab and imaging workup to identify source and monitor prognosis; lactic acid as a key marker of perfusion and severity.
• Treatment strategies for septic/septic shock:
  • Fluids to restore intravascular volume (crystalloids as first-line); vasopressors if hypotension persists after fluids.
  • Antibiotics promptly; vasopressors include Epinephrine and Dopamine (alpha and beta-adrenergic agonists).
  • Oxygen therapy and respiratory support as needed.
  • Antipyretics for fever and symptomatic support.
• Sepsis care in neutropenic patients: rapid administration of antibiotics is critical due to the high risk of rapid progression to multi-organ failure; any fever in immunocompromised patients warrants urgent evaluation.

Section 4: Cardiogenic Shock – Causes and Mechanisms

• Definition: cardiogenic shock results from the heart’s inability to pump effectively, leading to impaired tissue perfusion.
• Most common cause: myocardial infarction (heart attack) or acute coronary syndrome; dysrhythmias and myocarditis also contribute.
• Other etiologies: cardiomyopathy (enlarged heart), valvular disease with regurgitation, and congenital/structural defects affecting cardiac output.
• Pathophysiology: decreased cardiac output → systemic hypoperfusion → tissue hypoxia and organ dysfunction; compensatory mechanisms (tachycardia, vasoconstriction) may fail over time.
• Clinical relevance: signs and symptoms overlap with other shock types but the root cause is cardiac pump failure rather than fluid deficit or distributive vasodilation.
• Management considerations (brief): focus on improving cardiac output and tissue perfusion; use vasopressors for hypotension if needed and implement therapies appropriate for underlying cardiac pathology (revascularization, anti-ischemic therapies, arrhythmia management, etc.).

Section 5: Anaphylactic (Hemolytic) Shock – Allergic Reactions and Airway Compromise

• Trigger: severe allergic reaction (anaphylaxis) causing widespread vasodilation and increased capillary permeability.
• Key pathophysiology: dilation of blood vessels and leakage of fluid into interstitial spaces; airway constriction can lead to hypoxia and respiratory compromise.
• Immediate management emphasis:
  • Epinephrine administration is critical (often via IM auto-injector for public use; IV dosing in hospital settings may differ); patients should carry epinephrine (EpiPen) and have rapid access to emergency care after use.
  • If symptoms recur, a second dose may be needed; monitor for potential reactions or biphasic responses.
  • In hospital IV administration of epinephrine carries extravasation risk; ensure proper IV site management and monitoring for infiltration.
• Practical considerations: educate patients with severe allergies about carrying epinephrine and seeking urgent care after use; ensure access to second dose if symptoms return.

Section 6: Fluid Balance, Edema, and Hypervolemia vs Hypovolemia

• Third-spacing and edema: shifts of fluid from intravascular space to interstitial compartments; tissue swelling and risk of tissue compromise, particularly in limbs.
• Monitoring for fluid overload (hypervolemia): signs include edema, dyspnea, weight gain, and changes in respiratory status; prevent overcorrection when treating hypovolemia.
• Role of perfusion and urine output in monitoring: decreasing urine output signals reduced perfusion; restoration of perfusion should reverse some of the water shifts but require careful monitoring for overload.
• Special note on brain edema: when cerebral edema is present, pupillary response (PERLA) may be sluggish; brain edema is a marker of severe hypoperfusion and acidosis.

Section 7: Electrolytes, Sodium, and Related Interventions

• Core electrolytes discussed: sodium (Na), potassium (K), chloride (Cl), calcium (Ca); other electrolytes are not exhaustively listed in the transcript, but these are the focus here.
• Sodium: causes, signs/symptoms, treatment, and nursing interventions were highlighted as essential pharmacologic knowledge; hypotension and bradycardia are listed as potential signs requiring assessment of Na balance.
• Potassium (K): hypokalemia discussed in the context of fluid shifts and vomiting; signs and symptoms linked to heart and rhythm concerns; treatment includes IV fluid management and correction of underlying causes.
• Chloride (Cl): relevance in vomiting and acid-base disturbances; consider in electrolyte management discussions.
• Calcium (Ca): discussion connected to hypoglycemia and electrolyte balance; ensure calcium considerations in shock states where relevant.
• General approach to electrolyte management in shock:
  • Replete electrolytes while treating the underlying cause (dehydration, vomiting, diarrhea, renal dysfunction).
  • Monitor labs and adjust fluids accordingly; prevent rapid shifts that can cause arrhythmias or other complications.
  • Use nursing assessments to track fluid balance (weight, intake/output), vital signs, and neuro status.
• Practical study tip from instructor: suggest making flashcards with front: category (e.g., “Sodium balance”) and back: causes, signs, treatment, and nursing interventions; integrate with disease processes for deeper understanding.

Section 8: ABGs, Compensation, and Clinical Reasoning

• The instructor emphasizes understanding compensation and ABG concepts as part of exam readiness; not all ABG numbers are provided in the transcript, but the idea is to know how the body compensates for decreased perfusion (e.g., metabolic acidosis from lactic acid buildup, respiratory compensation attempts).
• Expect exam questions that test recognition of compensated vs decompensated states, ABG interpretation, and how compensation shifts with different shock types.

Section 9: Case Study Practice – Bow Tie Activity and Shock Identification

• Case setup: 39-year-old male with hematemesis, jaundice, hypertension, medical history of esophageal varices due to alcoholic hepatitis; prior GI bleed with banding; thrombocytopenia; comorbidity profile suggests advanced liver disease with portal hypertension.
• Task: identify the patient’s shock type, provide two interventions, and two monitoring actions.
• Instructor notes: emphasize teamwork in selecting the correct type of shock and the appropriate nursing interventions, including monitoring parameters specifically tied to the chosen shock category.
• Additional content touched: Stevens-Johnson syndrome risk with antibiotics (penicillin-containing Zosyn) and the need to monitor IV sites for extravasation when vasopressors are used; remind to review two vasopressors (epinephrine and dopamine) and their adrenergic effects.
• Important connection: the case integrates GI bleed, liver disease, coagulopathy (thrombocytopenia), and shock physiology to illustrate complex clinical decision-making in critical care.

Section 10: Exam-Focused Takeaways and Practical Reminders

• memorize the four major shock types discussed: Hypovolemic, Septic, Cardiogenic, Anaphylactic (the lecture also covered a distributive/shock framework and signs of perfusion failure).
• Key diagnostic/therapeutic anchors:
  • Early sepsis management: cultures + broad-spectrum antibiotics within 20 minutes of ER arrival; vasopressors for hypotension; fluids for perfusion; oxygen and supportive care.
  • Hypovolemic shock: prioritize isotonic fluids and source control; monitor urine output and weight; prevent over-resuscitation and edema.
  • Cardiogenic shock: identify underlying cardiac cause (MI, dysrhythmia, myocarditis, cardiomyopathy, valvular disease); support cardiac output with appropriate therapies.
  • Anaphylactic shock: rapid epinephrine administration, airway management, and post-episode observation.
• Practical nursing considerations:
  • Monitor orthostatic vitals to detect perfusion changes.
  • Track capillary refill, skin temperature, and signs of vasoconstriction for early detection of shock.
  • Watch for signs of cerebral edema (sluggish pupils) as a late or more severe sign of poor perfusion.
  • Educate patients about central lines and lines-associated infection risks; ensure patient education on home-use devices like EpiPen when applicable.

Section 11: Quick Reference Figures and Formulas (LaTeX)

• Urine output threshold for perfusion assessment: ext{Urine output} < 30\frac{\text{mL}}{\text{kg} \cdot \text{hr}}.
• Time to antibiotics in sepsis protocol: t \le 20\ \text{minutes}.
• Vasopressor examples and notes: Epinephrine and Dopamine are used to sustain blood pressure; both have adrenergic effects (alpha and beta agonism); monitor for extravasation if IV administration occurs.
• Notation used in discussions:
  • ANC: ANC < 500. (neutropenia threshold mentioned for high-risk infection scenarios)
  • Lactic acid elevation as a marker of sepsis/septic shock and tissue hypoperfusion.