a. Definition. Shock occurs when the circulatory system is unable to keep up with the metabolic demands of the body. The circulatory failure leads to reduced tissue perfusion causing cellular and tissue hypoxia. In addition to clinical evidence of tissue and end-organ hypoperfusion, shock commonly presents with hypotension (systolic blood pressure <90 mm Hg or a decrease in blood pressure from baseline exceeding 50 mm Hg).
Shock can also present without severe hypotension due to compensatory vasoconstriction.
b. Clinical manifestations of shock—regardless of etiology—usually include:
iii. Altered mental status
iv. Decreased urine output
v. Cool clammy skin (in nondistributive shock)
B. Causes of Shock. The many causes of shock must be remembered because treatment must address both the manifestations of shock and its underlying cause. The causes of shock are classified in four categories:
a. Distributive shock is characterized by severe pathologic vasodilation and reduction in systemic vascular resistance. Causes of distributive shock can be memorized using the “DEANS” list:
MNEMONIC: Causes of Distributive Shock (“DEANS”)
Drugs: primarily occur with vasodilating agents.
Endocrine is rare and includes causes such as mineralocorticoid deficiency in adrenal failure or myxedema coma.
Anaphylactic shock occurs due to immunoglobulin E (IgE)-mediated allergic reactions and is commonly associated with respiratory difficulties due to bronchospasm.
Neurogenic shock can be associated with severe traumatic brain injury or spinal cord injury and is thought to be related, in part, to autonomic alterations.
Sepsis is the most common cause of shock and results from a dysregulated immune response to an infectious process. Bacterial infections caused by gram-negative rods (e.g., Escherichia coli, Klebsiella, Proteus, Pseudomonas) or gram-positive cocci (e.g., Staphylococcus, Streptococcus) are common causes of septic shock. However, other infectious microorganisms (e.g., viruses, fungi) can also cause septic shock.
b. Hypovolemic shock. Any process that causes a significant reduction in intravascular volume can lead to hypovolemic shock. Causes include hemorrhage/bleeding, gastrointestinal losses (vomiting/diarrhea), cutaneous losses (burn patients, Stevens-Johnson syndrome), renal losses (excessive diuretics, salt-wasting nephropathies), and third spacing as occurs in severe pancreatitis, cirrhosis, or intestinal obstruction.
c. Obstructive shock is the least common cause of shock and is caused by disorders that impair cardiac blood return and filling such as cardiac tamponade, pulmonary embolism, or tension pneumothorax. These conditions should always be considered promptly because early emergent treatment is necessary to save the patient’s life.
d. Cardiogenic shock is most commonly the result of “pump failure,” caused by a myocardial infarction (of either the left or right ventricle), myocarditis, or dilated cardiomyopathy. Other cardiac causes include tachyarrhythmias or bradyarrhythmias, advanced valvular dysfunction (more pronounced with acute valve regurgitation), and mechanical complications such as rupture of the septum, ventricular wall, or papillary muscle.
e. Combined shock. It is not uncommon for patients to have multiple components of shock.
C. Approach to the Patient. The evaluation of the patient in circulatory failure is heavily dependent on the combination of clinical and hemodynamic assessment and supported by biochemical, imaging, and select procedural findings as required on a case-to-case basis.
a. Physical examination. The ABCs (airway, breathing, and circulation) should be assessed first. Physical examination findings can be helpful in confirming evidence of circulatory failure (mental status changes, decreased urine output, peripheral vasoconstriction) and identifying a possible etiology.
i. Blood pressure should be verified with a manual cuff. Hypotension is usually defined as a systolic pressure that is less than 90 mm Hg but can vary across individuals. Pulsus paradoxus (>10 mm Hg drop in systolic pressure with inspiration) suggests cardiac tamponade. A narrow pulse pressure can suggest low stroke volume as could be seen in cardiogenic shock, whereas in patients with suspected valve disease, a wide pulse pressure would raise suspicion for severe aortic regurgitation.
ii. Temperature. If the patient is febrile or hypothermic, septic shock gets higher on the differential.
iii. Oxygen saturation should be obtained during the initial assessment.
iv. Neck vein assessment. Elevated neck veins in a hypotensive patient are usually indicative of:
2. Tension pneumothorax
3. Large pulmonary embolism (with right ventricular failure)
4. Right ventricular infarction (typically associated with an inferior wall myocardial infarction)
5. Biventricular dysfunction (the only entity on this list that will also cause rales)
v. Lung sounds
1. Wet rales usually suggest a cardiac cause. Focal rales with egophony should lead you to think about sepsis from an underlying bacterial pneumonia.
2. Wheezing should increase suspicion of anaphylaxis.
3. Asymmetric breath sounds may represent pneumothorax or asymmetric/unilateral pleural effusions. Unilateral consolidation or pulmonary embolism can also lead to asymmetrically decreased breath sounds with auscultation.
vii. Abdominal palpation is helpful in evaluating whether pancreatitis, a perforated viscus, or an infected hepatobiliary source is the cause of shock. Hepatomegaly or hepatojugular reflux could be consistent with elevated filling pressure suggestive of cardiogenic failure in the appropriate clinical setting. Abdominal palpation can also help identify an abdominal aortic aneurysm (AAA), which can raise concern for AAA rupture.
viii. Rectal examination is important, especially if gastrointestinal bleeding is likely.
ix. Skin inspection. A scarlatiniform rash may be indicative of toxic shock syndrome, whereas urticaria can be a sign of anaphylaxis.
x. Neurologic examination is useful to assess mental status and to ensure that the patient does not have spinal cord compression.
b. Laboratory tests. Useful tests include:
i. A complete blood count (CBC).
ii. A chemistry panel, including blood urea nitrogen (BUN) and creatinine levels.
iii. Liver function tests.
v. Blood cultures.
vi. Arterial blood gases, including lactate level, which tends to be elevated in patients with shock.
vii. Central venous oxygen saturation (Scvco2).
c. A chest radiograph and electrocardiogram (EKG) are mandatory.
d. Other diagnostic modalities (e.g., computed tomography [CT], echocardiography, endoscopy, ventilation-perfusion [V/Q] scan, cardiac biomarkers, or evaluation of thyroid-stimulating hormone [TSH] level or serum cortisol) should be enlisted promptly if warranted by clinical suspicion.
e. In situations in which the cause of shock is not clear, pulmonary artery (PA) catheterization can be useful to identify the etiology of shock by providing data about volume status/filling pressures, cardiac output, and vascular resistance (Table 13.1). The PA catheter can also be useful in guiding appropriate therapy and assessing the response to intervention, particularly in cardiogenic shock patients.
Table 13.1 Pulmonary Artery Catheterization Findings in Specific Disease States
↑ or ↓
Few other disorders have a low SVR (distributive shock disorders)
Source of fluid loss must be identified
PCWP = CVP = PADP (equalization of pressures)
Normal to ↑
PADP is often 5 mm Hg > PCWP
Diagnosis is usually apparent on physical examination and chest x-ray
Right ventricular infarct
If the patient is hypoxemic and the chest x-ray is normal, consider a right-to-left shunt
Normal to ↓
Hemodynamics can be similar in adrenal insufficiency
CO = cardiac output, normal: 3.5–7 L/min; CVP = central venous pressure; PADP = pulmonary artery diastolic pressure, normal: 5–12 mm Hg; PASP = pulmonary artery systolic pressure, normal: 15–30 mm; Hg; PCWP = pulmonary capillary wedge pressure, normal: 5–12 mm Hg; RAP = right atrial pressure (equivalent to central venous pressure), normal: 0–8 mm Hg; SVR = systemic vascular resistance, normal: 900–1300 dynes/sec/cm–5.
D. Treatment. The goal of treating shock is to provide adequate hemodynamic support to ensure tissue perfusion and oxygenation and prevent end-organ dysfunction. Therefore, the initial management of shock is the same regardless of etiology, with focus on appropriate monitoring and resuscitation. Weil et al. summarized the initial steps of shock management using the mnemonic “VIP”: Ventilate (oxygenation), Infuse (fluid repletion), and Pump (vasoactive medication support) to achieve goal mean arterial pressure of 65-–70 mm Hg (to be adjusted and individualized depending on evidence of adequate tissue perfusion. For example, a lower target is acceptable in some patients with hemorrhagic shock or cardiogenic shock from severe aortic regurgitation). These treatment measures are usually instituted even before a definitive cause of shock has been identified.
a. Monitoring includes the use of intraarterial catheters for closer hemodynamic monitoring (especially if manual blood pressure measurements are unreliable) and blood gas assessment, insertion of urinary catheters for close monitoring of urine output, and frequent clinical and laboratory evaluation.
b. Respiratory support. Provide supplemental oxygen to improve oxygen delivery and minimize hypoxia-induced pulmonary vasoconstriction and worsening pulmonary vascular resistance. Mechanical ventilation should be considered in patients with severe hypoxemia, significant work of breathing, or persistent acidemia and in patients unable to protect their airway.
c. Fluid resuscitation. Rapid administration of fluids through large-bore intravenous catheters is necessary in all types of shock except for patients presenting in cardiogenic shock with evidence of elevated filling pressure and biventricular failure. Restoring euvolemia is the “pressor of choice” in patients who are intravascularly depleted. Fluids should be administered in boluses as opposed to slow maintenance infusion, usually starting with crystalloids, although colloids should be considered in some circumstances. Several methods can help decide fluid responsiveness, including passive leg-raise test, but repeated fluid challenges while assessing hemodynamic and end-organ function response are more commonly used. Care should be taken to avoid volume overload because that can worsen the respiratory status.
d. Vasoactive agents include vasopressors and inotropes, which are most commonly used, although in cardiogenic shock without systemic hypotension, vasodilators are also of utility to improve perfusion. The choice of which vasoactive agent to use depends on the clinical situation and should be guided by hemodynamic requirements and monitoring.
i. Mechanism of action. Vasoactive agents act on the autonomic nervous system. After you understand what each receptor does (Table 13.2), it is easy to remember the actions of each pressor.
Table 13.2 Vasopressors
2–64 mcg /min
Most types of shock
1–2 mcg /kg/min
2–5 mcg /kg/min
5–20 mcg /kg/min
Sepsis, hypotensive cardiogenic shock
1–10 mcg /min
ACLS, sepsis, anaphylaxis
1–20 mcg /kg/min
Cardiogenic shock (but not by itself if patient is hypotensive), congestive heart failure
1–4 mcg /min
* Action depends on the dose.
ACLS = advanced cardiac life support.
ii. Agents.Table 13.2 lists the most commonly used vasopressors in order from α1-adrenergic agents to β2-adrenergic agents.
1. Norepinephrine is the vasopressor of choice for most patients presenting with shock. Patients in cardiogenic shock due to “pump failure” without severe hypotension can be started on inotropes with or without vasopressors if necessary. (If you need a mnemonic to help you remember these vasoactive agents, you can think of the following scenario: paroxysmal nocturnal dyspnea [PND] is when a person wakes up gasping for breath as if just emerging from a DIVE)”.
MNEMONIC: Vasoactive agents (“PND DIVE”)
Dobutamine/phosphodiesterase inhibitors (milrinone)
Isoproterenol (not used in shock)
Table 13.3 Review of Autonomic Nervous System
Peripheral vascular and coronary smooth muscle
Increases heart rate and contractility
Bronchial, peripheral vascular, and coronary smooth muscle
Vascular smooth muscle (renal, gastrointestinal)
2. Vasopressin. Vasopressin, a hormone typically responsible for osmotic control in the renal collecting ducts, has been shown to have significant vasopressor effects through direct constriction of vascular wall smooth muscle cells. It is commonly used as a second agent.
In cardiogenic shock (and, less commonly, distributive shock), advanced mechanical support—including temporary ventricular-assist devices (intra-aortic balloon pump, Impella, Tandem Heart) in cardiogenic shock or extracorporeal membrane oxygenation (ECMO) in cardiogenic or distributive shock—can be considered.
e. Reversing the cause. While efforts to stabilize the patient and support hemodynamics are ongoing, finding and reversing the underlying cause of shock is critical. For example, in acute myocardial infarction with cardiogenic shock, reperfusion therapy is the most important intervention of proven mortality benefit. Likewise, thrombolysis in select patients with massive and hemodynamically unstable pulmonary emboli, draining a pericardial effusion in patients with tamponade, or using needle decompression in case of tension pneumothorax, can be life-saving. In septic shock, early goal-directed therapy, in addition to appropriate antimicrobial treatment and source control, is essential for improving survival.
Suggested Further Readings
Cardiovascular drugs in the ICU. Treat Guidel Med Lett 2002;1:19–24. (Classic Article.)Find this resource:
Cecconi M, De Backer D, Antonelli M, et al. Consensus on circulatory shock and hemodynamic monitoring. Task Force of the European Society of Intensive Care Medicine. Intensive Care Med 2014;40:1795–815.Find this resource:
Howell MD, Davis AM. Management of sepsis and septic shock. JAMA 2017;317:847–8.Find this resource:
Khanna A, English SW, Wang XS, et al. Angiotensin II for the treatment of vasodilatory shock. N Engl J Med 2017;377:419–30.Find this resource:
Landry DW, Oliver JA. The pathogenesis of vasodilatory shock. N Engl J Med 2001;345:588–95. (Classic Article.)Find this resource:
Vincent JL, De Backer D. Circulatory shock. N Engl J Med 2013;369:1726–34.Find this resource:
Weil MH, Shubin H. The “VIP” approach to the bedside management of shock. JAMA 1969;207:337–40. (Classic Article.)Find this resource: