Shock

What is the definition of shock?

Inadequate tissue perfusion leading to decreased oxygen delivery, anaerobic metabolism, increased lactic acid, metabolic acidosis, cell injury, and organ dysfunction

What is perfusion, and why does it matter in shock?

The delivery of oxygen and nutrients to tissues via blood flow; inadequate perfusion deprives cells of oxygen, forcing anaerobic metabolism and leading to organ dysfunction

What is mean arterial pressure (MAP), and what is a normal range?

The average arterial pressure during one cardiac cycle, roughly diastolic BP plus one third of the pulse pressure; normal MAP is about 70 to 100 mmHg, and a MAP below 65 mmHg is generally inadequate to perfuse vital organs

What is cardiac output, and how is it calculated?

The volume of blood the heart pumps per minute, calculated as heart rate multiplied by stroke volume

What is preload, and how does it relate to venous return?

The volume of blood stretching the ventricle at the end of diastole; it increases with venous return and affects stroke volume and cardiac output

What is afterload?

The resistance the heart must pump against to eject blood, largely determined by systemic vascular resistance

What is systemic vascular resistance (SVR), and what does it reflect?

The resistance blood vessels offer to blood flow, mainly determined by vessel diameter; vasoconstriction increases SVR and vasodilation decreases it, making SVR a major determinant of blood pressure and afterload

What is the difference between hypoxia and hypoxemia?

Hypoxia is decreased oxygen delivery to tissues; hypoxemia is decreased oxygen in the blood; hypoxemia can cause hypoxia, but tissue hypoxia can also occur with normal blood oxygen if perfusion is poor

What is the difference between aerobic and anaerobic metabolism, and why does shock trigger the anaerobic pathway?

Aerobic metabolism uses oxygen to produce ATP efficiently; anaerobic metabolism occurs without adequate oxygen, producing less ATP and generating lactic acid; shock decreases oxygen delivery, forcing cells into anaerobic metabolism

What is the goal of compensation in shock, and what systems are involved?

To maintain perfusion via neurohumoral activation, including the sympathetic nervous system (SNS), the renin angiotensin aldosterone system (RAAS), and antidiuretic hormone (ADH)

What is the difference between compensated and decompensated (progressive) shock?

In compensated shock, SNS, RAAS, and ADH responses maintain blood pressure and perfusion to vital organs; in decompensated shock, these mechanisms fail, leading to hypotension and organ hypoperfusion

What happens when compensation fails in shock?

Progressive ischemia leads to multi organ failure and death

Why is a normal blood pressure not always reassuring in early shock?

Compensatory mechanisms like tachycardia and vasoconstriction can maintain blood pressure despite significant volume loss or hypoperfusion, so other signs such as heart rate, skin perfusion, mental status, and urine output must be assessed

What is the fundamental imbalance that occurs in shock?

Oxygen demand increases or oxygen supply becomes insufficient, leading to inadequate tissue perfusion and cellular hypoxia

What is the stepwise progression of shock at the cellular level?

Decreased oxygen delivery leads to anaerobic metabolism, which increases lactic acid and causes metabolic acidosis, which causes cell injury, which leads to organ dysfunction

What is the initiating mechanism common to all types of shock?

Decreased circulating volume, decreased cardiac output, or decreased vascular tone, leading to tissue hypoperfusion

What happens during the cellular dysfunction phase of shock?

Decreased oxygen delivery causes anaerobic metabolism, increasing lactate and causing metabolic acidosis, which decreases ATP production

What is the vicious cycle that perpetuates shock?

Decreased ATP causes cellular injury, which causes inflammation and endothelial dysfunction, worsening hypoperfusion and leading to organ dysfunction

What characterizes the initial and compensatory stages of shock?

Initial: decreased cardiac output and oxygen delivery, triggering early anaerobic metabolism; compensatory: SNS, RAAS, and ADH activation causing increased heart rate, increased respiratory rate, vasoconstriction, and decreased urine output

What characterizes the progressive and irreversible stages of shock?

Progressive: compensatory mechanisms fail, leading to hypotension and organ hypoperfusion; irreversible: multi organ failure, ischemia, and death

What are the early and compensatory signs of shock, and their approximate MAP changes?

Early: MAP decreases about 10 mmHg from baseline, compensation still effective with increased oxygen delivery to vital organs and increased heart rate; compensatory (non progressive): MAP decreases 10 to 15 mmHg from baseline, with increased RAAS/ADH activity, vasoconstriction, increased pulse pressure, increased heart rate, decreased pH, restlessness, and apprehension

What are the progressive and refractory signs of shock, and their approximate MAP changes?

Progressive (intermediate): MAP decreases about 20 mmHg from baseline, with tissue/organ hypoxia, oliguria, weak rapid pulse, decreased pH, and sensory/neurologic changes; refractory (irreversible): excessive cell/organ damage, multi system organ failure, and decreased pH

What triggers the vascular (baroreceptor) response in shock, and what is the mechanism?

Baroreceptors in the carotid sinuses and aortic arch detect decreased blood pressure; decreased stretch activates the SNS, causing arteriolar vasoconstriction (increases SVR), venoconstriction (increases venous return, preload, and cardiac output), and blood redistribution to prioritize heart and brain perfusion

What happens with prolonged vasoconstriction during shock?

Sustained vasoconstriction decreases skin, renal, and GI perfusion; endothelial injury plus systemic inflammation activates coagulation, leading to microthrombi, clotting factor consumption, and disseminated intravascular coagulation (DIC)

What triggers the chemoreceptor response in shock, its mechanism, timeline, and limitation?

Peripheral chemoreceptors in the carotid and aortic bodies detect decreased oxygen, increased carbon dioxide, or decreased pH, stimulating the medulla to activate the SNS and increase heart rate, contractility, cardiac output, vasoconstriction, and respiratory rate; it acts within seconds for short term oxygenation, but if hypoxia persists, lactic acidosis develops and chemoreceptor fatigue occurs

What triggers the renal response in shock, the resulting cascade, and its early indicator and late effect?

Decreased renal perfusion causes juxtaglomerular cells to release renin (10 to 60 minutes), which converts to angiotensin I then angiotensin II, causing vasoconstriction and increased blood pressure, and stimulating aldosterone for sodium/water retention and increased volume; decreased urine output is an early indicator of renal hypoperfusion, and persistent ischemia can lead to acute tubular necrosis and renal failure as a late effect

What is the adrenal response in shock, including the SNS/adrenal medulla and HPA axis/cortisol pathways?

SNS stimulation of the adrenal medulla releases epinephrine and norepinephrine, increasing heart rate, contractility, and vasoconstriction for rapid perfusion support; the HPA axis stimulates the adrenal cortex to release cortisol, increasing catecholamine sensitivity and glucose availability for sustained support, though prolonged stress causes hyperglycemia and immunosuppression

What is the goal, mechanism, and critical threshold of the cerebral response in shock?

The goal is to maintain constant cerebral blood flow despite systemic hypotension, through autoregulation that dilates cerebral arterioles when MAP decreases or carbon dioxide increases; cerebral perfusion pressure (CPP) equals MAP minus intracranial pressure, with ischemia occurring if CPP falls below 60 mmHg, and prolonged hypotension causes loss of autoregulation, cerebral hypoxia, edema, decreased level of consciousness, and coma

What is the hepatic response to shock involving epinephrine and vasoconstriction?

Epinephrine stimulates glycogenolysis for glucose release as energy; vasoconstriction shunts blood flow to vital organs, risking hepatic ischemia

What is the metabolic role and risk of impaired hepatic function in shock?

Impaired lactate clearance and detoxification increase toxins, ammonia, and lactic acidosis, contributing to multi organ dysfunction syndrome (MODS)

What is the pulmonary response to acidosis in shock?

Tachypnea occurs as compensatory hyperventilation (Kussmaul type breathing) to decrease carbon dioxide, temporarily correcting pH and improving alveolar oxygen exchange

How can the pulmonary response progress to ARDS in shock?

Endothelial injury increases capillary permeability, causing pulmonary edema, decreased gas exchange, and progression to acute respiratory distress syndrome (ARDS)

What are the four major classifications of shock?

Hypovolemic (decreased volume), cardiogenic (pump failure), obstructive (flow obstruction), and distributive (vasodilation); all lead to inadequate tissue perfusion

What is the mechanism of hypovolemic shock, and what are its two main types?

Decreased intravascular volume decreases venous return (preload), decreasing cardiac output and tissue perfusion; types are hemorrhagic (trauma, GI bleed, aneurysm rupture, post surgical bleed) and non hemorrhagic (dehydration, burns, vomiting, diarrhea, diuresis, third spacing)

What is the clinical pearl regarding hypovolemic shock compensation?

Tachycardia, narrow pulse pressure, and cool clammy skin may precede hypotension and can be a compensatory response; a normal blood pressure does not exclude significant hypovolemia

What are the early signs and symptoms of hypovolemic shock?

Tachycardia, hypotension, narrow pulse pressure (decreased stroke volume), cool clammy pale skin (peripheral vasoconstriction), oliguria less than 0.5 mL/kg/hr, and anxiety/restlessness

What are the advanced signs and symptoms of hypovolemic shock?

Hypotension unresponsive to fluids with weak thready pulses, hypothermia, confusion progressing to lethargy and coma, and persistently decreased cardiac output despite fluid resuscitation with decreased mixed venous oxygen saturation

What laboratory findings are seen in hypovolemic shock?

Decreased hemoglobin/hematocrit (after fluid shift, may be normal early), increased lactate, increased BUN/creatinine ratio greater than 20 to 1 (prerenal azotemia), increased sodium/osmolality, metabolic acidosis, and coagulopathy (increased PT/INR, decreased platelets) in hemorrhagic shock

What imaging and evaluation are used to diagnose hypovolemic shock?

FAST exam to detect intra abdominal bleeding, CT or angiography to localize internal hemorrhage, chest and pelvic X ray to identify fractures or bleeding sources, and continuous hemodynamic/urine output monitoring

What is the treatment approach for hypovolemic shock?

Fluid resuscitation starting with crystalloids (NS or LR), activating the massive transfusion protocol (1:1:1 PRBC:FFP:platelets) if hemorrhagic, hemostatic measures (control bleeding source, direct pressure, early tranexamic acid), monitoring (MAP at least 65 mmHg, urine output, lactate), norepinephrine only after adequate volume restoration, and correcting the underlying cause

What is the pathophysiologic pathway of cardiogenic shock?

Decreased cardiac contractility (pump failure) leads to decreased cardiac output, increased left ventricular filling pressures, pulmonary congestion and hypoxia, and decreased systemic perfusion (multi organ hypoperfusion)

What is the vicious cycle of cardiogenic shock?

Decreased cardiac output decreases coronary perfusion, increasing myocardial ischemia, which further decreases contractility

What are the common causes of cardiogenic shock?

Myocardial infarction (most common), cardiomyopathy (dilated, hypertrophic), arrhythmias (ventricular tachycardia, high grade heart block), and valvular disease (mitral regurgitation, aortic stenosis)

What are the classic hemodynamic findings in cardiogenic shock?

Decreased cardiac output and cardiac index, increased filling pressures (PCWP at least 18 mmHg, increased CVP), and increased systemic vascular resistance (compensatory); the classic pattern is decreased CO, increased PCWP, increased SVR

What is the clinical presentation of cardiogenic shock?

Chest pain, dyspnea/orthopnea/crackles from pulmonary congestion, cyanosis and cool clammy skin, decreased urine output, JVD and hepatic congestion if right ventricular failure, weak/thready pulses, hypotension, tachycardia, and altered mental status

What diagnostic findings support cardiogenic shock?

ECG showing ST elevation or arrhythmia, echocardiogram showing decreased LVEF/wall motion abnormalities/decreased stroke volume, labs showing increased troponin/BNP/lactate, and CXR showing pulmonary congestion or cardiomegaly

What is the treatment for cardiogenic shock?

Inotropes (dobutamine or milrinone) to increase contractility and cardiac output, vasopressors (norepinephrine) to maintain MAP at least 65, diuretics (furosemide) to decrease pulmonary congestion, revascularization (PCI or CABG) for MI related shock, mechanical support (IABP or LVAD) for refractory cases, and avoiding fluid overload

What is the pathophysiologic pathway of obstructive shock?

Mechanical obstruction to cardiac filling or output decreases venous return (preload), decreasing cardiac output and tissue perfusion

What are the common causes of obstructive shock?

Pulmonary embolism (increased RV afterload), tension pneumothorax (mediastinal shift decreasing venous return), cardiac tamponade (increased pericardial pressure decreasing filling), and aortic dissection (compromised major arterial flow)

What are the hemodynamic findings in obstructive shock?

Decreased cardiac output, decreased preload, increased right atrial pressure/CVP, and increased SVR (compensatory)

What is the clinical presentation of obstructive shock?

Sudden severe hypotension with tachycardia and weak thready pulses, dyspnea/tachypnea/cyanosis, distended neck veins/JVD, cool clammy skin, restlessness/anxiety/altered LOC, and pulsus paradoxus (notably in tamponade)

What specific findings characterize cardiac tamponade and tension pneumothorax?

Tamponade: muffled heart sounds, narrow pulse pressure, increased JVD with clear lungs; tension pneumothorax: absent breath sounds on the affected side, tracheal deviation, sudden hypoxia

What specific findings characterize pulmonary embolism and aortic dissection as causes of obstructive shock?

Pulmonary embolism: pleuritic chest pain, tachypnea, hypoxia, possible hemoptysis; aortic dissection: sudden tearing chest or back pain, pulse deficits, differential blood pressure between arms

What diagnostics are used for obstructive shock?

ECG showing right heart strain or electrical alternans, echo showing RV dilation or pericardial effusion, CT angiography for PE or aortic dissection, and CXR for pneumothorax

What is the treatment for each cause of obstructive shock?

PE: tPA or catheter thrombolysis then heparin/LMWH; tension pneumothorax: immediate needle decompression then chest tube; tamponade: pericardiocentesis, surgical window if recurrent; dissection: urgent surgery plus blood pressure control with a beta blocker

What is the pathophysiologic pathway of distributive shock?

Widespread vasodilation (decreased SVR) causes blood pooling (increased capacitance), decreasing venous return (preload) and cardiac output

What are the three subtypes of distributive shock?

Septic, anaphylactic, and neurogenic

What are the hemodynamic findings and skin changes in distributive shock?

Increased or normal cardiac output, decreased SVR, and decreased preload; skin is warm initially from vasodilation, becoming cool as hypoperfusion progresses

What is the pathophysiology of septic shock?

Infection triggers a cytokine storm (TNF alpha, IL

What are the two clinical phenotypes of septic shock?

Hyperdynamic (warm) phenotype with normal or increased CO, decreased SVR, warm flushed skin, bounding pulses, and widened pulse pressure; hypodynamic (cold) phenotype with decreased CO, impaired tissue perfusion, cool mottled skin, weak pulses, and possibly narrow pulse pressure

What laboratory findings support a diagnosis of septic shock?

Lactate at least 2 mmol/L (at least 4 mmol/L indicates higher risk), leukocytosis or leukopenia, elevated procalcitonin, positive blood cultures (often gram negative), elevated CRP/ESR, metabolic acidosis, and organ injury labs (increased BUN/creatinine, LFTs, bilirubin, troponin)

What is the treatment approach for septic shock?

Broad spectrum antibiotics within one hour then tailored to cultures, 30 mL/kg crystalloid fluids, norepinephrine first line vasopressor (add vasopressin if needed), source control (drain abscess, remove infected devices), monitoring goals (MAP at least 65, lactate clearance of 10 to 20% in 2 to 6 hours, urine output greater than 0.5 mL/kg/hr), and hydrocortisone if refractory to pressors

What is the pathophysiology of anaphylactic shock?

IgE mediated mast cell/basophil degranulation after allergen exposure releases histamine, tryptase, leukotrienes, and prostaglandins, causing vasodilation (decreased SVR), increased capillary permeability (decreased preload), bronchoconstriction, and airway edema

What is the clinical presentation of anaphylactic shock?

Rapid onset within minutes after exposure, with skin findings (urticaria, flushing, pruritus, angioedema), respiratory findings (wheezing, stridor, dyspnea), cardiovascular findings (hypotension, tachycardia, syncope), and GI findings (nausea, vomiting, cramping, diarrhea)

What is the immediate treatment for anaphylactic shock?

Epinephrine IM (0.3 to 0.5 mg of 1:1000 concentration) in the mid anterolateral thigh, repeated every 5 to 15 minutes, as first line; airway and oxygen support; rapid isotonic crystalloid fluids (1 to 2 L); adjuncts (H1 antihistamine, H2 blocker, corticosteroid); and observation for at least 4 to 6 hours for biphasic reaction risk

What is the definition and mechanism of neurogenic shock?

Distributive shock from loss of sympathetic tone, commonly after spinal cord injury at or above T6; loss of sympathetic tone causes unopposed vagal activity, systemic vasodilation (decreased SVR), and decreased venous return, resulting in decreased cardiac output and blood pressure with bradycardia as the hallmark finding

What are the early clinical findings of neurogenic shock?

Decreased blood pressure with bradycardia (hallmark), warm dry flushed skin below the injury, flaccid paralysis with decreased reflexes and anhidrosis below the lesion, normal or decreased JVD, and hypothermia from vasodilation and impaired thermoregulation

What are the progressive clinical findings of neurogenic shock?

Dizziness, syncope, decreased level of consciousness, decreased urine output, respiratory compromise if the injury is above C5, and decreased sweating below the lesion

How does neurogenic shock differ from spinal shock?

Neurogenic shock results from loss of sympathetic tone with vasodilation and bradycardia, whereas spinal shock is a transient loss of all neurologic function (motor, sensory, and reflex) after spinal cord injury; they can coexist but are not the same

What is the treatment for neurogenic shock?

Cautious IV fluid replacement (500 to 1000 mL crystalloid) to optimize preload, maintaining MAP at least 85 mmHg to ensure spinal cord perfusion while avoiding fluid overload, norepinephrine (preferred) or phenylephrine for vasopressor support, atropine for symptomatic bradycardia, spinal stabilization/decompression as indicated, respiratory support for high cervical injury, and preventing secondary injury

What is multiple organ dysfunction syndrome (MODS), and what are its key clinical findings?

Persistent hypoperfusion plus systemic inflammation causing dysfunction of two or more organ systems; key findings include oliguria, altered level of consciousness, respiratory failure, and hepatic dysfunction (increased liver enzymes)

What is disseminated intravascular coagulation (DIC) as a complication of shock, and what are its key clinical findings?

Widespread coagulation activation causing microthrombi and consumption of clotting factors; key findings include bleeding (oozing, diffuse), petechiae, decreased platelets, increased D

What is acute respiratory distress syndrome (ARDS) as a complication of shock, and what are its key clinical findings?

Inflammatory alveolar capillary injury causing pulmonary edema and impaired gas exchange; key findings include severe hypoxemia, dyspnea/increased work of breathing, and bilateral pulmonary opacities on CXR

What is the overall clinical pearl connecting shock to its major complications?

Shock causes sustained tissue hypoperfusion plus inflammation, leading to cellular injury and organ dysfunction (MODS); early goal directed restoration of perfusion is critical to prevent progression to MODS, DIC, and ARDS