Shocks
Sepsis Wrap Up
Overview of Circulatory Shock
Definition: Circulatory shock is an umbrella term for all forms of shock causing hypoperfusion of organs and tissues.
Leads to insufficient nutrient and oxygen supply to meet metabolic demands.
Resultant processes include ischemia, anaerobic metabolism, and tissue necrosis.
Types of Circulatory Shock:
Distributive Shock: Three categories:
Septic Shock
Anaphylactic Shock
Neurogenic Shock (e.g., due to spinal cord injury or severe head injury leading to systemic vasodilation)
Hypovolemic Shock: Due to significant blood or plasma volume loss.
Cardiogenic Shock: Resulting from heart dysfunction.
Obstructive Shock: Caused by external obstruction to the heart's pumping ability.
Histamine's Role in Allergic Reactions
Function: Histamine is the main mediator of allergic inflammation.
Mechanism:
Binds to H1 receptors on endothelial and smooth muscle cells, increasing vascular permeability and leading to edema.
Causes leakage of white blood cells and plasma (exudate) into surrounding tissues.
Results in changes in osmotic pressure, promoting fluid movement out of circulation.
Causes stagnation of blood flow due to low-pressure systems from vasodilation and activates platelets, increasing clotting risks.
Effects:
Blood stasis and endothelial injury leading to intrinsic coagulation cascades.
Release of Platelet Activating Factor (PAF) from mast cells, leading to bronchoconstriction.
Prostaglandins are also involved in the inflammatory response.
Allergens and Their Reactions
Definition: An allergen (also referred to as an antigen) is a substance that triggers an allergic response.
Common Allergens:
Drugs:
Penicillins, Sulfa antibiotics, blood products, morphine (whole blood is the highest risk, albumin is the lowest).
Foods:
Nuts, shellfish, and others.
Venoms:
From wasps, ants, etc.
Latex:
First exposure leads to specific IgE synthesis; second exposure induces an IgE-mediated immune response usually within 15 minutes.
Allergy to Anaphylaxis Continuum
Symptoms of Allergy:
Pruritus (itchiness)
Urticaria (hives)
Lacrimation (watery eyes)
Rhinitis (runny nose)
Angioedema
Pathophysiology of Anaphylaxis:
Allergen binds to IgE, causing mast cell degranulation and the release of histamine and various cytokines, complements, leukotrienes, bradykinins, and nitric oxide.
Examples include:
Localized Allergy:
Wasp sting causes localized swelling and urticaria without compromising airway, breathing, circulation (ABCs).
Inhaled Allergens:
Dander exposure results in rhinitis and watery eyes without compromising ABCs.
Symptoms of Allergic Reactions
Common Symptoms Include:
Rash
Lacrimation
Runny nose
Sneezing
Red eyes
Itching
Clinical Considerations in Allergic Reactions
Questions to Consider:
Which drug class is applicable to allergy-mediated inflammation?
In cases of localized allergy, what would be the treatment approach?
If the allergy progresses (generalized itching, slight concern, normal vital signs), how would you assess for worsening conditions?
Anaphylaxis
Definition: Anaphylaxis is a severe, potentially life-threatening systemic response characterized by significant vasodilation and bronchoconstriction.
Symptoms may include warmth and a flushed appearance as a result of vasodilation, hypotension, and respiratory compromise.
Treatment Protocol for Anaphylaxis:
Epinephrine:
Administered intramuscularly as first-line treatment.
Causative agents must be stopped (e.g., transfusion reactions require stopping blood product administration).
Glucocorticoids:
Dexamethasone IV is given for longer-term management (not life-saving).
Post-stabilization: consider prescribing oral prednisone for 3 days and an EpiPen.
2nd generation antihistamines may be used as adjunctive therapy.
Phase of Anaphylaxis: It's critical to understand different stages, with hypoperfusion and fluid shifts leading to circulatory collapse potentially causing up to 35% volume loss within 10 minutes.
General Treatment Approach:
ABCs: Administer high-flow oxygen and consider intubation, if necessary.
Utilize beta-2 adrenergic agonists (e.g., Salbutamol) for bronchospasm management.
Administer Epinephrine via IV if needed following the initial IM dose, along with fluid resuscitation using Normal Saline (NS) boluses.
Hypovolemic Shock
Definition: Hypovolemic shock occurs due to a significant decrease in blood or plasma volume, leading to inadequate filling of vascular compartments and decreased cardiac output.
Defined by an acute loss of 20% or greater volume.
Causes:
Blood loss from trauma, surgery, burns, etc.
Low extracellular fluid resulting from severe dehydration due to low intake, vomiting, or diarrhea.
Physiology: Initial volume loss triggers sympathetic nervous system (SNS) compensation to maintain perfusion; continued losses lead to decompensation and shock.
Signs and Symptoms of Hypovolemic Shock
Initial Symptoms:
Consistent with compensatory mechanisms:
Tachycardia
Thirst
End-organ vasoconstriction (e.g., cool, pale integument)
Oliguria (urine output < 20ml/hour)
Drenching diaphoretic skin
Normal blood pressure maintained by SNS.
Progressive Symptoms:
Hypotension (SBP < 90 mmHg)
Thready pulse indicative of vasoconstriction and low blood pressure
Decreased respiratory rate
Central nervous system changes like irritability, restlessness, or altered levels of consciousness (confusion progressing to coma).
Signs of cellular dysfunction may manifest as electrolyte imbalances or hyperglycemia.
Shock Classification: Septic vs. Anaphylactic vs. Hypovolemic
Septic and Anaphylactic Shock:
General appearance on survey may be flushed and warm due to vasodilation.
Hypovolemic Shock Appearance:
Characterized as cool and pale/mottled due to vasoconstriction, causing accelerated ischemic events.
Treatments for Hypovolemic Shock
IV Fluids: Utilize crystalloid solutions (Normal Saline - NS, Lactated Ringer's - LR), colloids (Albumin 5% or 25%, Dextran), or blood products (PRBCs, whole blood, fresh frozen plasma - FFP).
Monitoring Parameters: Essential to monitor perfusion status, blood pressure, and pulse. Be cautious of potential circulatory overload due to excessive fluid administration.
Urine Output Tracking: Maintain clear records of input/output (I&O) to assess kidney function.
Clearance Calculation: Monitor renal function through appropriate calculations.
Cautions: There exists a risk for allergic reactions to colloids and blood products, and dilutional coagulopathy may arise from high crystalloid volumes.
Complications of Hypovolemic Shock
Main Complications:
Hypoxia: leading to impaired cellular function.
Metabolic Acidosis: Due to lactate accumulation leading to organ dysfunction/failure.
Multi-Organ Dysfunction Syndrome (MODS): Affects multiple systems including renal failure and impacts brain function.
Gastrointestinal Ischemia: Can arise as blood flow is redirected away from the gut.
Lung Injury (ARDS): Results in pulmonary hypoperfusion, inflammation, pulmonary edema, and may lead to respiratory failure.
Renal Impacts: Renal failure and electrolyte imbalances frequently require treatment, including possible renal dialysis to substitute for renal function.
Renal Function: Effects and Treatments
Erythropoietin (EPO) Production:
EPO is a hormone produced in the kidneys that stimulates RBC synthesis in the bone marrow. This is crucial for maintaining oxygen-carrying capacity. Low EPO production results in decreased RBC levels and potential hypoxemia.
Vitamin D Activation:
The kidneys activate Vitamin D, which in its active form, calcitriol, facilitates calcium absorption in the gastrointestinal tract and kidneys.
Cardiogenic Shock
Etiology: Commonly results from myocardial infarction (particularly STEMI), arrhythmias, cardiac insufficiency, or other shocks impacting cardiac function.
Operational Dynamics: This shock type indicates ineffective cardiac output to meet body demands despite appropriate total blood volume; it emphasizes that Left Ventricular Cardiac Output (LV CO) equals Right Ventricular Cardiac Output (RV CO).
Treatment Overview for Cardiogenic Shock
Goals: Primarily aims to optimize cardiac output through the following strategies:
Reduce both preload and afterload while enhancing contractility through various pharmacologic interventions and fluid management:
Diuretics:
Spironolactone, a potassium-sparing diuretic, decreases sodium retention through aldosterone antagonism.
Furosemide (Lasix) for rapid diuresis with caution in hypotension.
Vasodilators:
Direct-acting vasodilators like nitroglycerin and nitroprusside may improve coronary circulation but require monitoring for hypotension.
Synergistic strategies with ACE inhibitors, adrenergic antagonists, and calcium channel antagonists can improve hemodynamics.
Inotropic Agents:
Phosphodiesterase inhibitors (e.g., Milrinone) and catecholamines (e.g., Dobutamine) for contractility enhancement but with caution regarding vasoconstriction.
Temporary Management of Cardiogenic Shock
Advanced Treatment:
Intra-aortic balloon pump (IABP): A device that is 26 cm long, inserted into the descending aorta through a catheter.
Function: Inflates during diastole and deflates before systole, enhancing blood flow through a suction effect, particularly beneficial in acute ischemic events.
Obstructive Shock
Definition: Characterized by mechanical obstruction to blood flow in the central circulation.
Etiology Examples:
Large embolisms (e.g., pulmonary embolism - PE) and cardiac tamponade are primary causes.
Management Strategies:
Address the underlying issue:
For cardiac tamponade, perform pericardiocentesis.
For PE, employ anticoagulants, thrombolytics, and consider aspiration of the obstruction.
Invasive Procedures:
Aspiration thrombectomy via femoral venous access may be required to remove life-threatening pulmonary emboli.