MD Notes

creation date: 2025-05-01 18:49
tags: PathologiesIncomplete

Shock

Background

Definitions

Shock is defined as a life-threatening condition of circulatory failure. It is a state of cellular tissue hypoxia due to inadequate oxygen delivery for the metabolic demands.

The effects of shock are initially reversible but can deteriorate to an irreversible state with multiorgan failure and death.

Four types of shock are recognized, of which multifactorial shock is possible:

  • Distributive (62% septic shock, 4% other)
  • Cardiogenic (16%)
  • Hypovolemic (16%)
  • Obstructive (2%)

Etiology and Pathogenesis

Cellular hypoxia occurs as a result of reduced perfusion and/or increased oxygen consumption or from inadequate oxygen utilization.

Cellular hypoxia results in a positive feedback loop involving ion pumps, pH, and leakage that results in a cascade of worsening tissue perfusion. Tissue hypoxia is results in elevated serum lactate levels as a result of anaerobic metabolism.

Distributive shock

Characterized by severe peripheral vasodilation. Capillary leakage may cause redistribution of fluid from intravascular to extravascular comparment. The molecules that mediate vasodilation vary based on etiology.

Cardiac output may increase initially but with drop in preload and cardiac depression, CO decreases.

Septic shock

  • A subset of sepsis, which is defined as a dysregulated host response to infection resulting in capillary leakage and systemic vasodilation
  • Circulating inflammatory cytokines causes myocardial depression
  • Types of pathogens varies and ranges from gram-positive bacteria (eg. Pneumococcus, Enterococcus), gram-negative organisms (eg. Pseudomonas, Klebsiella, Enterobacter), antibiotic-resistant organisms (eg. MRSA), and fungi (eg. Candida).
    Systemic inflammatory response syndrome (SIRS)
  • Characterized by robust inflammatory response
  • Induced by infectious (similar to septic shock) or noninfectious (eg. pancreatitis, blunt trauma, air/fat/fluid embolism)
    Neurogenic shock
  • Interruption of autonomic pathways due to severe brain and/or spinal cord injury results in unopposed vagal tone
  • Vagal tone causes peripheral vasodilation and pooling of peripheral blood
    Anaphylactic shock
  • Severe immunoglobulin-E mediated allergic reaction resulting in degranulation of mast cell
  • Massive histamine release causes vasodilation and capillary leakage
    Drug and toxin-induced shock
  • SIRS-like syndrome can be induced by drug overdoses (eg. narcotics), snake/insect/spider bites, heavy-metal poisoning, transfusion reactions
  • Cyanide and carbon monoxide causes shock from mitochondrial dysfunction
    Endocrine shock
  • Addisonian crisis (due to mineralocorticoid deficiency) and myxedema
  • In mineralocorticoid deficiency, vascular tone is altered
  • In myxedema, link to thyroid hormone unclear

Cardiogenic shock

Characterized by intracardiac causes of cardiac pump failure → decreased cardiac contractility and/or stroke volume → decreased cardiac output

Cardiomyopathic

  • Consist of failure of cardiac myocardium
  • Most common cause is myocardial infarction (typically requires at least 40% of LV to be affected or any amount if there is significant ischemia or other conditions such as heart failure)
  • Other causes include hypertrophic cardiomyopathy or diastolic heart failure but these rarely result in shock
    Arrhythmic
  • Both atrial and ventricular tachyarrhythmias and bradyarrhythmias can contribute to shock
  • Can become shock is CO is compromised significantly such as with complete heart block
  • CO can also become absent due to underlying rhythm (eg. pulseless VTach, Vfib)
    Mechanical
  • Mitral valve insufficiency or due to valvular defects from rupture of papillary muscle or chordae tendineae.
  • Aortic insufficiency due to retrograde dissection into aortic valve ring or abscess of aortic ring
  • Severe ventricular septal defects or rupture of intraventricular septum

Hypovolemic shock

Loss of intravascular fluid → decreased preload and stroke volume → decreased cardiac output
Hemorrhagic

  • Shock due to a reduction in intravascular volume from blood loss
  • Can be due to blunt or penetrating trauma, upper, and lower GI bleed (in order of prevalence).
  • Less common causes include intra- and postoperative bleeding, ruptured aneurysm, and more
    Non-hemorrhagic
  • Loss of fluid other than blood
  • Could be from GI (eg. diarrhea, vomitting), skin loss (eg. burns), renal loss (eg. salt-wasting nephropathies), or third space losses into extravascular space or body cavities

Obstructive shock

Obstruction of heart or great vessels → inability for heart to circulate blood → decreased cardiac output
Pulmonary vascular

  • Due to right ventricular failure from hemodynamically significant pulmonary embolism or severe pulmonary hypertension and heart is unable to overcome pulmonary resistance
    Mechanical
  • A number of causes can cause mechanical obstruction which includes tension pneumothorax, cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathy.

Clinical Presentation

Signs & Symptoms

Stages of shock

Shock begins with an inciting event and progresses through several stages. Early stages are more likely to be reversible and treatable while end-stage shock is associated with irreversible end-organ damage.

Pre-shock: aka compensated shock

  • Characterized by compensatory responses to diminished tissue perfusion
  • Eg. hypovolemic shock may see tachycardia and peripheral vasoconstriction
    Shock:
  • Characterized by compensatory mechanisms being overwhelmed and signs of organ dysfunction appear
  • Signs may include:
    • Symptomatic tachycardia
    • Dyspnea
    • Restlessness
    • Diaphoresis
    • Metabolic acidosis
    • Hypotension
    • Oliguria
    • Cool, clammy skin
      End-organ dysfunction
  • Irreversible organ damage, multiorgan failure, and death
  • At this stage, anuria and acute kidney failure develop, acidemia further depresses cardiac output, hypotension becomes severe, and hyperlactatemia worsens
  • Restlessness evolves into obtundation and coma

Clinical features

In addition to general findings, specific features vary based on the classification of shock.

Vitals:

FeatureClassic findingExceptions
Heart rateIncreasedNormal if on ß-blocker; decreased in neurogenic shock and some cardiogenic (eg. ß-blocker overdose)
Blood pressureDecreased (<65 mmHg or 40 mmHg under baseline)Normal in hypertension superimposed or early sepsis
Resp rateIncreasedDecreased in obtunded patients (eg. severe shock or intoxication)
SpO2NormalDecreased with hypoxemia (eg. pulmonary disease, tissue hypoxia (eg. severe shock w/ peripheral O2 consumption); falsely low if severe peripheral vasoconstriction
Pulse pressureDecreasedIncreased in distributive shock

Distributive shock:
Presents with hypotension with reduced preload or fluid overload:

  • Skin turgor is normal
  • Mucous membranes are moist
  • IVC normal on imaging
  • Preserved or hyperdynamic left ventricle on echocardiography
  • No peripheral edema
  • No distended neck veins
  • Central venous pressure is normal (8-12 mmHg)
  • Mixed venous oxyhemoglobin saturation (SvO2) >70%

Septic shock

  • Symptoms suggestive of source of infection
  • Cutaneous manifestation of infective endocarditis
  • Fever
    Anaphylactic shock
  • Flushing
  • Urticaria
  • Hoarseness of voice
  • Oral and facial edema
  • Exposure to common allergens

Cardiogenic shock:
Presents with hypotension with manifestation of:

  • Pulmonary edema
  • Elevated CVP (>12 mmHg)
  • Low SvO2 (<70%)
  • Large, dilated ventricles and poor LV function
  • Valvular or septal abnormalities on echocardiography
    Specific findings also present based on etiology (eg. findings of MI)

Hypovolemic shock:
Presents with characteristic reduced preload with suspected/known cause:

  • Reduced skin turgor
  • Dry mucous membranes
  • Collapsible IVC on imaging
  • Low CVP (<8 mmHg)
  • Orthostatic hypotension
  • Pallor
  • Flattened JVP
  • Sequelae of chronic liver disease
    Findings may vary additionally based on hemorrhagic or nonhemorrhagic etiology.

Obstructive shock:
Presents with hypotension usually without signs of fluid overload or reduced preload but with distended neck veins.

  • Subacute cardiac tamponade may have signs of fluid overload
  • Pericardial tamponade may find effusion on imaging
  • PE or ptx may have dilated RV and small LV

Combined findings:
Note, forms of shock can coexist and may induce each other. As a result, clinical findings may not match specifically.

Empiric treatment for specific causes of shock may be needed to determine predominant form.

History & Physical Exam

It is important to maintain a high clinical suspicion for shock, especially if symptoms are present.

Focused history from patient (if possible) and/or family/friends should be used to determine the type of shock. For example:

  • History of infection leading to sepsis
  • Exposure to allergens, medications, food items, insect stings

In cases of suspected SIRS/sepsis, the SIRS, Sepsis, and Septic Shock Criteriacan be used for risk stratification and work-up algorithm.

Shock index (SI) can be calculated rapidly to assess risk of shock, typically in trauma cases. Shock index = HR / SBP

  • SI of 0.5-0.7 is considered normal
  • SI > 0.9 considered elevated
  • Rising SI can be an indication of worsening shock

Objective exam should include assessment of sensorium, mucous membranes, lips and tongues, neck veins, lungs, heart, abdomen, skin, and joints.

Risk factors

Risk factors vary based on type of shock.

Septic shock:

  • Suppressed immune system
  • Extremes of age (infants or elderly)
  • Procured organ (transplant)
  • Surgical procedure
  • Indwelling devices
  • Sickness

Cardiogenic shock:

  • Advanced age
  • Asian and pacific Islanders
  • Heart and blood vessel problems
  • Diabetes
  • Obesity
  • Past history of coronary artery bypass grafting (CABG)
  • Pneumothorax
  • Sepsis

Hypovolemic shock:

  • Trauma
  • GI problems (eg. ulcer, bleed)
  • Surgery
  • Ectopic pregnancy
  • Burst aneurysm

Diagnosis

Criteria

Shock is a clinical diagnosis. Work-up is used to determine etiology and direct treatment.

In most patients the following are present:

  • Tissue hypoperfusion
  • Oliguria
  • Altered mental status
  • Hyperlactatemia

Work-up

Initial steps to undifferentiated hypotension/shock should be done simultaneously with resuscitation and stabilization efforts once clinical condition is consistent with shock.

Following a brief history and examination, bedside telemetry, electrocardiography, and point-of-care ultrasonography should be used to assess whether immediate or early lifesaving therapy is needed.

  • Collapsed IVC on POCUS suggests fluid depletion and fluid challenge should be considered

A number of POCUS algorithms are available, including the Rapid Ultrasound for Shock and Hypotension (RUSH) exam for undifferentiated shock and Focused Assessment with Sonography for Trauma (FAST) exam for trauma.

Laboratory evaluation should be done as soon as possible:

  • Serum lactate
    • 2 mmol/L generally considered elevated
  • Metabolic panel (incl. kidney and liver function tests)
    • Elevated BUN, creatinine, and transaminases due to end-organ damage
    • Serum and urinary electrolytes may indicate hypovolemia
  • Cardiac enzymes and natriuretic peptides
    • Elevated troponin, BNP, or NT-pro-BNP may indicate cardiogenic shock
  • Complete blood count and differential
    • High hematocrit suggests hypovolemia
    • Anemia in setting of bleeding supports hemorrhagic shock
    • Elevated eosinophil may suggest anaphylaxis
    • Low WBC may suggest sepsis
  • Coagulation studies and D-dimer
    • Elevated PT, INR, or PTT may point towards an etiology for hemorrhagic shock; may also be elevated in sepsis/SIRS
    • D-dimer can be used to rule out PE and aortic dissection
  • Blood gas analysis
    • ABG may aid in assessing gas exchange and acid-base disturbances
    • VBG may be considered as it can be drawn with initial labs

A chest radiograph is performed to detect common causes such as pneumonia, pneumothorax, pulmonary edema, or widened mediastinum. Further radiographs and CTs may be considered based on suspected etiology.

Differential

The primary differential consist of the various etiologies of shock.

BRASH syndrome: bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia combined to form rare, life-threatening condition; each component worsens other components cyclically.

Other causes of hypotension include:

  • Chronic hypotension
  • Drug-induced hypotension
  • Autonomic dysfunction
  • Vasovagal syncope
  • Peripheral vascular disease

Red Flags / Complications

Untreated shock can lead to end-organ damage and can be life threatening:

  • Septic shock - mortality of 40-50%
  • Cardiogenic shock - mortality of 50-75%

Management

Initial Management

First step consist of:

  • Securing the airway with oxygen and/or mechanical ventilation (most patients require intubation but not all require mechanical ventilation; exception of tension ptx)
  • Establish IV access for laboratory studies

IV fluids should be considered following IV access.

  • Administer bolus of IVF as fluid challenge
  • Consider aggressive fluids and blood products for those with obvious hemorrhage (eg. gunshot wound)
  • If cardiogenic shock is suspected, fluids should not be administered - consider diuresis with volume overload (eg. IV furosemide)

Balanced crystalloids are preferred over normal saline (0.9% sodium chloride) due to their electrolyte composition closer to physiologic plasma (normal saline is supraphysiological) which reduces the risk of adverse kidney events.

  • Lactated Ringer’s
  • Plasma-Lyte

Life-saving or early intervention and stabilization

Based on brief history and exam, bedside telemetry, ECG, and POCUS, assess whether stabilizing intervention is needed.

Common interventions include:

  • Tension pneumothorax - chest tube
  • Cardiac tamponade - pericardiocentesis
  • Anaphylaxis - IM epinephrine 0.3-0.5mg (1:1000, 1 mg/mL)
    • q 5min prn up to 3 times before IV epinephrine
    • Exact dosing: 0.01 mg/kg up to maximum of 0.5mg per dose
  • Overwhelming sepsis - IV antibiotics
    • If Pseudomonas unlikely:
      • Vancomycin plus third or fourth-generation cephalosporin
      • Beta-lactam/beta-lactamase inhibitor (eg. pip-tazo)
      • Carbapenem (eg. imipenem, meropenem)
    • If Pseudomonas likely:
      • Vancomycin plus two antipseudomonal agents (eg. fluoroquinolone, pip-tazo)
  • Adrenal crisis - IV hydrocortisone 100 mg
  • Hemorrhage - drainage or emergent surgery
  • Hemodynamically significant arrhythmias - cardioversion, atropine, pacemaker placement, inotrops etc. following ACLS protocols
  • Myocardial infarction - antiplatelet and/or cardiac cath
  • Ruptured valve - surgical repair
  • Pulmonary embolism - thrombolysis

Distributive shock

Cardiogenic shock

The goal of treatment is to:

  1. Restore perfusion (avoiding reducing BP, manage volume, antithrombotic if needed)
  2. Restore inotropy following reperfusion (using inotrops)

Dysrhythmias
With pulse:

  • Bradycardia - synchronized cardioversion and IV atropine
  • Tachycardia - synchronized cardioversion
    Without pulse:
  • Asystole or PEA - CPR (not shockable)
  • V-tachy/Vfib - CPR and defibrillation

Valvulopathies

  • Surgery

Hypovolemic shock

Obstructive shock

Treatment of underlying etiology

Continue empiric therapies for presumed etiologies until patient is stabilized. Response to therapies should be monitored and refined as diagnosis is elucidated.

Resuscitation is continued as needed. This consist of:

  • IV fluids
  • Vasopressors (first-line: norepinephrine)

References

Tools / Guidelines

MDCalc - SIRS/Sepsis/Septic Shock Criteria
Uptodate - Approach algorithms

Additional Reading

Backlinks