Shock

What is shock?

A state of circulatory failure leading to inadequate tissue perfusion.

What are the four major types of shock?

Cardiogenic, distributive, hypovolemic, and obstructive.

What does an elevated PCWP indicate?

Left-sided heart failure, volume overload, or mitral valve disease.

What is Cardiac Output (CO)?

The volume of blood pumped by the heart per minute.

What does Central Venous Pressure (CVP) reflect?

Right ventricular preload.

What is the formula for Mean Arterial Pressure (MAP)?

MAP = 1/3 SBP + 2/3 DBP.

What is the standard MAP target?

≥ 65mm Hg

Why is diastolic BP important in cardiogenic shock?

Critical for coronary perfusion.

What is the clinical significance of a MAP below 60 mm Hg?

Organ perfusion declines linearly.

What is the relationship between oxygen delivery and shock?

Shock results from an imbalance between oxygen delivery (DO₂) and oxygen demand.

What are the consequences of decreased oxygen delivery in shock?

Cellular hypoxia, anaerobic metabolism, and lactate production.

What are the clinical hallmarks of shock?

Hypotension, tachycardia, altered mental status, decreased urine output, and cool or warm extremities.

What goes wrong in shock?

Decreased CO, decreased SVR, and decreased effective oxygen delivery, leading to tissue hypoxia. All shock states ultimately lead to impaired DO2

What are the key clinical lactate markers in shock?

Elevated lactate: marker of tissue hypoperfusion

Clearing lactate: Improvement

What are the causes of cardiogenic shock?

Post-MI, end-stage HF, papillary muscle rupture, or lethal arrhythmias.

What are the signs of cardiogenic shock?

High CVP/PCWP, low CO, and high SVR.

What are the causes of distributive shock?

Sepsis (most common), anaphylaxis, neurogenic (loss of sympathetic tone)

What characterizes distributive shock?

Low SVR, high or normal CO, and warm extremities.

What are the causes of hypovolemic shock?

Hemorrhage (trauma/GI bleed), or non-hemorrhagic (burns, severe dehydration).

What is the profile of hypovolemic shock?

Low CVP, low CO, and high SVR.

What are the causes of obstructive shock?

Cardiac tamponade, tension pneumothorax, massive PE.

What physical signs are associated with obstructive shock?

High CVP, low CO, and signs like Pulsus Paradoxus or Beck's Triad.

What does decreased PCWP suggest?

Hypovolemia or distributive states. It helps differentiate cardiogenic vs non-cardiogenic causes of shock and pulmonary edema.

What is the significance of stroke volume in shock?

Stroke volume depends on preload, contractility, and afterload.

What are the parameters of cardiogenic shock?

CO: Decreased

SVR: Increased

Extremities: Cold, clammy

What are the parameters of distributive shock?

CO: Increased or normal

SVR: Decreased

Extremities: Warm, flushed

What are the parameters of hypovolemic shock?

CO: Decreased

SVR: Increased

Extremities: Cold, clammy

What are the parameters of obstructive shock?

CO: Decreased

SVR: Increased

Extremities: Cold, clammy

What are the three bedside assessment windows for assessing perfusion?

Neurologic (AMS, confusion, obtundation), cutaneous (mottling, prolonged capillary refill, cool/clammy) , and renal (oliguria).

What does oliguria indicate in shock?

A sign of renal hypoperfusion, defined as urine output <0.5 mL/kg/hr.

Can shock exist without overt hypotension?

Yes, always assess for end-organ hypoperfusion.

What is cardiogenic shock?

A cardiac disorder resulting in sustained tissue hypoperfusion, indicated by SBP < 90 mmHg for >30 min or need for vasopressors.

What is the most common cause of cardiogenic shock?

Acute myocardial infarction (MI), accounting for ~60-70% of cases historically.

What is the in-hospital mortality rate for cardiogenic shock?

Remains greater than 30% despite standard therapy.

What is the pathophysiology of cardiogenic shock?

Primary insult leads to decreased SV, causing decreased CO which leads to decreased MAP. Compensatory mechanisms like sympathetic activation caused increased HR, SVR and fluid retention.

What is the classic hemodynamic profile of cardiogenic shock?

Decreased cardiac index (CI ≤ 2.2 L/min/m²), increased pulmonary capillary wedge pressure (PCWP > 15 mmHg), increased systemic vascular resistance (SVR).

What is the most common phenotype of cardiogenic shock?

Cold and wet (about 2/3 of cases)

What are common etiologies of cardiogenic shock?

Acute MI, acute decompensation of chronic heart failure, acute myocarditis, and lethal arrhythmias.

What are the stages of SCAI shock classification?

Stage A: At Risk; Stage B: Beginning; Stage C: Classic; Stage D: Deteriorating; Stage E: Extremis.

What differentiates end organ damage in the SCAI shock classification?

Moving from stage B to stage C, and the presence of hypoperfusion.

What labs should be ordered for a cardiogenic shock workup?

Lactate (key marker of hypoperfusion), troponin, BNP/NT-proBNP, CBC, BMP, LFTs, ABG/VBG.

What is the first line imaging for cardiogenic shock?

Echocardiography.

What is the first assessment done in cardiogenic shock?

Volume assessment, cautious fluid challenge if no congestion; avoid overloading.

What is the first-line vasopressor for hypotension in cardiogenic shock?

Norepinephrine.

What is dopamine therapy associated with in cardiogenic shock?

More tachyarrhythmias.

What is epi therapy associated with in cardiogenic shock?

Higher refractory shock rates.

What is strongly discouraged as a sole first-line agent in cardiogenic shock?

Pure vasopressors.

What is the role of inotropes in cardiogenic shock management?

Dobutamine and milrinone are used to maintain systemic perfusion.

When is mechanical circulatory support (MCS) indicated in cardiogenic shock?

Indicated when pharmacologic therapy fails to maintain end-organ perfusion. Devices include intra-aortic balloon pump, impella, and VA-ECMO.

What signs should be recognized early in cardiogenic shock?

Hypotension, hypoperfusion and cardiac dysfunction.

What is the pathophysiology of distributive shock?

Pathologic vasodilation leading to decreased systemic vascular resistance (SVR) and relative hypovolemia despite normal or elevated cardiac output.

What is the most common type of shock in the ICU?

Distributive shock.

What is the definition of septic shock?

Sepsis with persisting hypotension requiring vasopressors to maintain MAP ≥ 65 mmHg and lactate > 2 mmol/L despite adequate fluid resuscitation.

What is the pathophysiology of septic shock?

Infection -> systemic inflammatory response -> massive cytokine release -> NO-mediated vasodilation -> decreased SVR.

What is the significance of the Frank-Starling mechanism in septic shock?

It allows for preserved stroke volume despite decreased ejection fraction in sepsis-induced cardiomyopathy.

What is the characteristic progression in septic shock?

"Warm shock" early (vasodilated, bounding pulses) can progress to "cold shock" (myocardial depression, vasoconstriction)

What are the clinical features of septic shock?

Fever or hypothermia, tachycardia, tachypnea, altered mental status, and oliguria.

What are the common lab findings in septic shock?

Increased lactate, leukocytosis or leukopenia, increased procalcitonin, coagulopathy, and increased creatinine.

What is the initial fluid resuscitation protocol for septic shock management?

At least 30 mL/kg IV crystalloid within the first 3 hours; use balanced crystalloids (lactated Ringer's) over normal saline.

What is the first-line treatment for septic shock?

Norepinephrine. Target MAP ≥65 mmHg.

What is added in septic shock management if NE dose reaches 0.25-0.5?

Vasopressin.

What is the effect of vasopressors in septic shock?

They help restore mean arterial pressure (MAP) and improve organ perfusion.

What is the antibiotic management strategy in septic shock?

Antibiotics within 1 hour of recognition, broad spectrum then narrow.

What is the pathophysiology of anaphylactic shock?

IgE-mediated massive mast cell degranulation causing histamine, tryptase release, leading to profound vasodilation, capillary leak and bronchospasm.

What are the clinical features of anaphylactic shock?

Urticaria, angioedema, wheezing/stridor, hypotension, and gastrointestinal symptoms.

What is the first-line treatment for anaphylactic shock?

Epinephrine administered intramuscularly. Observe for biphasic reaction (4-6 hours MINIMUM)

What is the pathophysiology of neurogenic shock?

Loss of sympathetic tone (usually from spinal cord injury above T6) leads to unopposed vagal tone causing vasodilation and bradycardia.

What distinguishes neurogenic shock from other shock types?

Hypotension and BRADYCARDIA, and warm, dry skin below level of injury.

What is the management for neurogenic shock?

IV fluids, vasopressors (norepi and phenylephrine to restore SVR), and atropine for symptomatic bradycardia.

What do all types of distributive shock have in common?

Decreased SVR is the primary hemodynamic derangement.

What is the pathophysiology of hypovolemic shock?

Decreased intravascular volume -> decreased preload -> decreased stroke volume -> decreased CO.

What are the 2 categories of hypovolemic shock?

Hemorrhagic and non-hemorrhagic

What can cause hemorrhagic hypovolemic shock?

Trauma, GI bleeding, ruptured AAA, surgical bleeding, postpartum hemorrhage.

What can cause non-hemorrhagic hypovolemic shock?

Severe dehydration (vomiting, diarrhea), burns (third-spacing), pancreatitis, diabetic ketoacidosis.

What is the hemodynamic profile of hypovolemic shock?

Decreased central venous pressure (CVP), decreased PCWP, decreased cardiac output (CO), and increased SVR.

What is the ATLS classification for hemorrhagic shock?

Class I: 15% blood loss; Class II: 15-30%; Class III: 30-40%; Class IV: >40%.

What are the clinical features of hypovolemic shock?

Tachycardia (earliest sign), cool/pale/clammy skin, flat neck veins, and delayed capillary refill.

What are the common lab findings in hypovolemic shock?

Increased lactate, increased BUN/Cr ratio, decreased Hgb (may be delayed in acute hemorrhage), metabolic acidosis.

In what class of hypovolemic shock will BP begin to decrease?

Stage III, after 1500-2000mL of blood loss (30-40% of blood volume loss)

What is the management for hemorrhagic hypovolemic shock?

Control the source of bleeding, massive transfusion protocol. TXA within 3 hours of injury, avoid excessive crystalloid.

What is the management for non-hemorrhagic hypovolemic shock?

Aggressive IV crystalloid resuscitation (with balanced crystalloids like Lactated Ringer's) and treat underlying cause.

What is checked to monitor for adequacy of resuscitation in hypovolemic shock?

Lactate levels, urine output (≥0.5 mL) and hemodynamic response to fluid challenges.

What is the significance of lactate clearance in shock management?

A target ≥20% reduction over 2 hours indicates improving tissue perfusion and is associated with reduced mortality.

What does a passive leg raise (PLR) predict?

If cardiac output will increase with volume expansion.

What indicates fluid responsiveness during a passive leg raise?

≥10% increase in cardiac output.

What is pulse pressure variation used to predict?

Fluid responsiveness in mechanically ventilated patients.

What percentage change in arterial pulse pressure indicates fluid responsiveness?

>12%

Why should CVP alone be avoided as a predictor of fluid responsiveness?

It is a poor predictor.

What is often the earliest sign of hypovolemic shock?

Tachycardia

What is the pathophysiology of obstructive shock?

Mechanical obstruction to cardiac filling or output -> decreased CO, despite adequate intravascular volume and myocardial function.

What is the hemodynamic profile of obstructive shock?

Increased CVP, decreased cardiac output, increased systemic vascular resistance (SVR).

What are the three classic causes of obstructive shock?

Cardiac tamponade, tension pneumothorax, massive pulmonary embolism.

What is the pathophysiology of cardiac tamponade?

Pericardial fluid accumulation leads to increased intrapericardial pressure, compressing cardiac chambers and decreasing venous return.

Does rate of accumulation or volume of accumulation matter more in cardiac tamponade?

Rate of accumulation, rapid and small volume can cause tamponade while slow and large volume may be tolerated.

What is Beck's Triad?

Hypotension, distended neck veins (increased JVP), muffled heart sounds.

What is pulsus paradoxus?

>10 mmHg drop in SBP during inspiration.

What are the hemodynamics found in cardiac tamponade?

Equalization of diastolic pressures across all chambers on PA catheter.

What is found on the echo in cardiac tamponade?

Pericardial effusion, RA collapse in late diastole, RV collapse in early diastole, respiratory variation in mitral inflow.

What is the treatment for cardiac tamponade?

Pericardiocentesis

What is the pathophysiology of tension pneumothorax?

Air trapped in the pleural space under pressure causes mediastinal shift and decreased venous return.