Shock study guide previews.

Shock management often fails not because clinicians don’t know what shock is - but because we make predictable cognitive and physiologic errors under pressure. This leads to include Escalating vasopressors without reassessing tissue perfusion and Ignoring signs of ongoing hypoperfusion despite “normal” blood pressure. Pearl include A “normal” MAP does not guarantee adequate oxygen delivery and Mistake #2: Giving Fluids to Every Shock Patient. Reflexively giving repeated fluid boluses to all hypotensive patients.

Anaphylactic Shock is a severe, life-threatening systemic hypersensitivity reaction characterized by distributive shock due to massive vasodilation, increased vascular permeability, and airway compromise. The mechanism involves igE-mediated mast cell/basophil degranulation leading to release of histamine, tryptase, leukotrienes, prostaglandins, cytokines. Key features include Hypotension (vasodilation + third-spacing), Airway compromise (bronchospasm, edema), and Cutaneous symptoms (urticaria, angioedema). The onset is usually sudden - typically minutes after allergen exposure. Common triggers include food (peanuts, shellfish), medications (antibiotics, NSAIDs, contrast), insect stings, latex.

The classic clinical pattern includes respiratory findings such as Dyspnea, wheezing, stridor, throat tightness, cardiovascular findings such as Hypotension, tachycardia, distributive shock picture, cutaneous findings such as Urticaria, flushing, angioedema, and GI cramps, vomiting, diarrhea, sense of impending doom.

The primary defect is widespread release of vasoactive mediators leading to decreased SVR, increased capillary permeability, relative hypovolemia, and bronchoconstriction.

It reflects microcirculatory blood flow, not just blood pressure. Prolonged CRT is associated with worse outcomes in shock, particularly septic shock. When used serially and correctly, CRT can guide resuscitation decisions and may help avoid over-resuscitation. Capillary refill time is the time (in seconds) it takes for color to return to a compressed capillary bed after pressure is released. Importantly include CRT assesses flow, not pressure, A patient can be normotensive yet have abnormal CRT (occult shock), and How to Measure CRT (Proper Technique Matters).

Choose the site include Distal phalanx of the index finger (most common), fingertip pulp, sternum (especially in darker skin tones or cold extremities), Release pressure, and Measure the time until normal color returns using a stopwatch or visual count.

Normal CRT (adults) include Generally ≤2 seconds (some protocols accept ≤3 seconds, especially in older adults). Prolonged CRT include seconds is typically considered abnormal in critical care contexts. Clinical pearl include CRT is most useful when measured the same way, at the same site, by the same team, over time. CRT reflects peripheral vasoconstriction, which occurs when the body prioritizes perfusion of vital organs (heart, brain) over skin and muscle.

Cardiogenic Shock is shock due to primary cardiac pump failure, leading to inadequate cardiac output despite normal intravascular volume. Key features include decreased cardiac output (CO), increased preload (CVP, PCWP) due to blood backing up, and increased SVR (compensatory vasoconstriction). Common etiologies include Acute myocardial infarction (especially STEMI), Arrhythmias (tachy- or bradyarrhythmias), Cardiomyopathy (dilated, restrictive), Acute valvular failure (papillary muscle rupture, severe MR/AR), and Myocarditis, stunned myocardium after cardiac arrest.

Bedside assessment may show Hypotension, tachycardia (though bradyarrhythmias possible) and Narrow pulse pressure. Bedside assessment may show Cool, clammy extremities (low perfusion), Jugular venous distension (increased right-sided filling pressures), Pulmonary edema (crackles, hypoxia, pink frothy sputum), and S3 gallop may be present. Bedside assessment may show Elevated troponins if MI-related, Lactate increased (global hypoperfusion), and decreased LV ejection fraction, wall motion abnormalities, or valvular pathology. The primary defect is pump failure leading to decreased stroke volume leading to decreased CO leading to decreased MAP leading to poor tissue perfusion.

Compensatory response includes increased SVR (via catecholamines) leading to worsens LV afterload. End result include Low forward output leading to tissue hypoperfusion, Elevated left-sided pressures leading to pulmonary congestion and edema, and Oxygen delivery impaired by both low output and impaired myocardial oxygen supply-demand balance.

Comprehensive Overview of Shock is shock is a life-threatening state of circulatory failure resulting in inadequate tissue perfusion and oxygen delivery.

The underlying physiology includes decreased O₂ delivery (DO₂) due to decreased cardiac output (CO), decreased systemic vascular resistance (SVR), decreased circulating volume, or obstruction to flow, Leads to cellular hypoxia, anaerobic metabolism, lactate production, acidosis, and ultimately multi-organ failure, and Hypotension, tachycardia, altered mentation, oliguria, poor capillary refill, elevated lactate.

Sepsis + cardiomyopathy, trauma with bleeding + tension pneumo. Universal Problem includes inadequate tissue oxygen delivery relative to demand. Two Core Pathways include decreased CO (cardiogenic, hypovolemic, obstructive) and Normal/increased CO but decreased effective perfusion (distributive). Downstream Effects include Anaerobic metabolism leading to lactate, Acidosis leading to impaired enzyme/cellular function, and End-organ failure (renal, hepatic, CNS).

Distributive Shock is a type of shock caused by loss of vascular tone and maldistribution of blood flow, leading to impaired tissue perfusion despite adequate or even increased cardiac output.

Key features include decreased systemic vascular resistance (SVR), cardiac output (CO) often preserved or increased, CO may decline due to myocardial depression and exhaustion, Described as “relative hypovolemia” since circulating blood volume is normal but ineffective due to dilation of the vascular compartment, and Septic shock.

Vital Signs include Hypotension (MAP <65 mmHg), Wide pulse pressure due to low diastolic pressure, and Tachycardia (except neurogenic shock leading to bradycardia). Bedside assessment may show warm, flushed skin, bounding pulses, rapid capillary refill (“warm shock”) and cool, mottled extremities, poor cap refill as hypoperfusion worsens. Bedside assessment may show Elevated lactate = marker of tissue hypoxia and high ScvO₂ due to impaired O₂ extraction. The primary defect is pathologic vasodilation leading to decreased SVR leading to inadequate perfusion.

Endocrine Shock is shock states caused by hormonal deficiencies or crises that impair vascular tone, cardiac output, or metabolism.

Most Important Etiologies include Adrenal crisis (Addisonian crisis): Cortisol with or without aldosterone deficiency leading to decreased vascular tone, decreased sodium/water retention, Myxedema coma (severe hypothyroidism): decreased myocardial contractility, bradycardia, decreased SVR, Thyroid storm (severe thyrotoxicosis): High-output failure leading to eventually decreased effective perfusion, Hypoglycemia (severe, prolonged): Impaired substrate delivery to tissues leading to neurologic collapse, circulatory dysfunction, and Unlike other forms of shock, endocrine-related shock is often diagnosed after common causes are ruled out.

Myxedema Coma include Hypothermia, bradycardia, hypotension and Altered mental status, dry skin, delayed reflexes. Thyroid Storm include Fever, tachycardia/arrhythmia, agitation, heart failure leading to later hypotension/shock. Hypoglycemia include Sweating, altered mental status, seizures, coma and Hypotension in severe/prolonged cases. Adrenal Crisis include decreased Cortisol leading to loss of catecholamine sensitivity leading to vasodilation and hypotension and decreased Aldosterone leading to sodium loss, hypovolemia, hyperkalemia. Myxedema Coma include Severe hypothyroidism leading to decreased contractility, bradycardia, decreased SVR and Accumulation of mucopolysaccharides leading to pericardial effusion, hypoventilation.

Hemorrhagic Shock is a type of hypovolemic shock caused by acute blood loss leading to decreased preload, decreased stroke volume, decreased cardiac output leading to impaired tissue perfusion. Key features include decreased intravascular volume (absolute), decreased preload (CVP/PCWP), Compensatory increased SVR (to preserve perfusion), and decreased CO if volume loss >15-20%. Common Causes include Trauma (penetrating/blunt), GI bleeding (variceal, ulcer, diverticular), Ruptured aneurysm or ectopic pregnancy, and Perioperative bleeding. Vital Signs include Hypotension (progresses with blood loss), Tachycardia (early compensatory), and Narrow pulse pressure.

Bedside assessment may show Cool, clammy skin (peripheral vasoconstriction), Delayed capillary refill, Jugular veins flat (low CVP), and Overt signs of bleeding (hematemesis, melena, trauma). Laboratory/POC Clues include Lactate increased (tissue hypoperfusion), Hb/Hct may be normal initially (dilution lags), and FAST exam/CT for trauma, endoscopy for GI bleed. The primary defect is loss of circulating blood volume leading to decreased preload leading to decreased stroke volume leading to decreased cardiac output.

Hemodynamic Cascade include Volume depletion, decreased venous return (CVP, PCWP), decreased stroke volume leading to decreased CO leading to decreased MAP, Compensatory increased SVR (vasoconstriction, catecholamine release), and Tissue hypoxia leading to anaerobic metabolism leading to lactate leading to acidosis leading to coagulopathy leading to shock spiral (“lethal triad”: acidosis, hypothermia, coagulopathy).

Hypovolemic Shock is a form of shock due to decreased intravascular volume, leading to inadequate preload, decreased stroke volume, and ultimately decreased cardiac output leading to impaired tissue perfusion. Key features include decreased preload (CVP, PCWP), decreased stroke volume and CO, and Compensatory increased SVR (to maintain perfusion). Etiology include Trauma, GI bleed, ruptured aneurysm and Vomiting, diarrhea, burns, diuresis, third-spacing (pancreatitis, peritonitis). Bedside assessment may show Hypotension (progressive as volume loss worsens), Tachycardia (early compensatory response), and Narrow pulse pressure.

Bedside assessment may show Cool, clammy skin (due to vasoconstriction), Delayed capillary refill, and Dry mucous membranes, decreased skin turgor (esp. in non-hemorrhagic). Bedside assessment may show Elevated lactate, Hemoconcentration in non-hemorrhagic losses, and Low hemoglobin/hematocrit in hemorrhage (may lag early). The primary defect is decreased Intravascular volume leading to decreased venous return (preload).

Hemodynamic Cascade include decreased preload (CVP/PCWP), decreased stroke volume leading to decreased CO, decreased MAP leading to tissue hypoperfusion, Compensatory increased SVR (catecholamine-driven vasoconstriction), and Cellular hypoxia leading to anaerobic metabolism leading to lactate production leading to metabolic acidosis.

In clinical practice, we are measuring lactate (not lactic acid). At physiologic pH, lactate is the dominant form. Lactate is not just a hypoxia marker. It reflects cellular stress, metabolic flux, adrenergic drive, mitochondrial function, and clearance capacity. In the ED and ICU, lactate is best used for Risk stratification (higher = worse prognosis), and and Trending over time (lactate clearance or persistence). Lactate includes the conjugate base produced from pyruvate; reported by labs in mmol/L.

Hyperlactatemia includes elevated lactate level (with or without acidosis). Lactic acidosis includes elevated lactate plus metabolic acidosis (low pH, low bicarbonate). Important nuance include You can have elevated lactate without acidemia and You can have metabolic acidosis without elevated lactate (e.g., ketoacidosis, renal failure). Why this matters include This reaction regenerates NAD⁺, allowing glycolysis to continue and Lactate production can rise even with adequate oxygen if glycolysis outpaces mitochondrial oxidation.

Lactate is an energy substrate, especially for the heart and brain. Clinical pearl includes elevated lactate reflects overproduction, under-clearance, or both. Occurs when oxygen delivery fails to meet demand.

Best practice includes consider using both together, especially in shock. Key point include Lactate is not a direct measure of perfusion. Key point include CRT is a real-time bedside marker of perfusion.

Neurogenic Shock is a type of distributive shock caused by loss of sympathetic tone following spinal cord injury (SCI), usually above T6.

The underlying physiology includes Loss of sympathetic outflow leading to unopposed parasympathetic (vagal) activity, Results in hypotension (vasodilation) + bradycardia (unique among shock types), and Must differentiate from spinal shock (neurologic syndrome of flaccid paralysis, areflexia, sensory loss below injury - not hemodynamic shock).

Common triggers include cervical or high thoracic SCI (trauma, tumor, iatrogenic). Vital Signs include Hypotension (decreased SVR), Bradycardia (decreased sympathetic input, increased vagal tone), and Hypothermia (loss of vasoconstriction & heat regulation). Bedside assessment may show Warm, dry extremities (contrast with hypovolemic shock leading to cool/clammy), paralysis, loss of sensation below lesion, and Absent reflexes acutely (spinal shock overlap). The primary defect is loss of sympathetic nervous system leading to widespread vasodilation and impaired cardiac stimulation.

Obstructive Shock is a form of shock caused by a mechanical obstruction to blood flow (either into or out of the heart), leading to inadequate cardiac output and tissue hypoperfusion. Key features include Normal intravascular volume and contractility, decreased cardiac output due to impaired filling or outflow, and increased SVR (compensatory). Common etiologies include Pulmonary embolism (PE), severe pulmonary hypertension and Cardiac tamponade, constrictive pericarditis. Bedside assessment may show Hypotension, tachycardia and Narrow pulse pressure (often).

Bedside assessment may show Beck’s triad - hypotension, JVD, muffled heart sounds. Pulsus paradoxus may be present. Bedside assessment may show Elevated lactate (global hypoperfusion).

Examples include Obstruction of pulmonary arteries leading to RV strain/failure leading to decreased LV preload, Pericardial fluid under pressure leading to prevents diastolic filling, and decreased preload or increased afterload leading to decreased cardiac output leading to hypotension and shock.

Key concept include Normal blood pressure does not equal adequate cardiac output. LV cannot overcome afterload leading to decreased stroke volume.

Shock Index is ratio of heart rate (HR) to systolic blood pressure (SBP). Why it matters includes sI is a simple bedside tool for assessing hemodynamic instability, often outperforming HR or SBP alone in detecting occult shock. Abnormal includes ≥ 0.9 - associated with increased risk of shock, need for massive transfusion, ICU admission, and mortality. Very high includes ≥ 1.3 - 1.5 leading to strongly predicts poor outcomes. SI > 0.9 associated with increased likelihood of significant hemorrhage and need for massive transfusion.

Elevated SI suggests decompensation and higher mortality risk. MSI > 1.3 may indicate risk of decompensation in obstetric hemorrhage. Less reliable in isolated tachyarrhythmias or hypertensive emergencies. Must interpret in clinical context; not diagnostic by itself. SI ≥ 1.3: high risk of mortality/ICU need.