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Health Dictionary

Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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Shock resident survival guide

Introduction

Overview

Overview

Shock is the syndrome of circulatory failure that results in inadequate cellular oxygen utilization. The diagnosis of shock is based on clinical signs (eg, altered mental status, oliguria, cold and clammy skin) and biochemical abnormalities (eg, hyperlactatemia, base deficit) indicative of tissue hypoperfusion.^[1] Management of shock consists of stabilization of the hemodynamic status and correction of the underlying cause.

Causes

Causes

Life Threatening Causes

Shock is a life-threatening condition and must be treated as such irrespective of the underlying cause.

Common Causes

Cardiogenic Shock

Arrhythmic

Mechanical

Myopathic

Pharmacologic

Obstructive Shock

Decreased cardiac compliance

Decreased ventricular preload

Increased ventricular afterload

Hypovolemic Shock

Fluid depletion

Hemorrhage

Distributive Shock

Click here for the complete list of causes.

FIRE: Focused Initial Rapid Evaluation

FIRE: Focused Initial Rapid Evaluation

A Focused Initial Rapid Evaluation (FIRE) should be performed to identify patients in need of immediate intervention.^[2]

Boxes in the salmon color signify that an urgent management is needed.

Abbreviations: CBC, complete blood count; CI, cardiac index; CK-MB, creatine kinase MB isoform; CVP, central venous pressure; DC, differential count; ICU, intensive care unit; INR, international normalized ratio; LFT, liver function test; MAP, mean arterial pressure; MVO2, mixed venous oxygen saturation; PCWP, pulmonary capillary wedge pressure; PT, prothrombin time; PTT, partial prothrombin time; SaO2, arterial oxygen saturation; SBP, systolic blood pressure; SCVO2, central venous oxygen saturation; SMA-7, sequential multiple analysis-7.

Does the patient have cardinal findings that increase the pretest probability of shock?

❑ Evidence of hypoperfusion

❑ Altered mental status

❑ Cool extremities

❑ Sustained hypotension

❑ SBP <90 mm Hg or

❑ MAP ↓ >30 mm Hg below baseline for ≥30 min

YES

NO

Ventilate—Infuse—Pump (VIP)

❑ Oxygen ± intubation with mechanical ventilation

❑ Normal saline 300–500 mL over 20–30 min

❑ ± Norepinephrine 0.1–2.0 μg/kg/min

Consider alternative conditions
(eg, chronic hypotension, syncope)

Workup

❑ ECG monitor

❑ Pulse oximeter

❑ Arterial blood gas

❑ Central venous catheter

❑ CBC/DC/SMA-7/LFT/PT/PTT/INR

❑ Troponin, CK-MB

❑ Chest radiograph

❑ Echocardiography

❑ Foley catheter

❑ ICU admission

❑ ± Transfusion (Indications)

❑ ± Cultures of blood, urine, etc.

❑ ± Pulmonary artery catheter (Indications)

Immediate Goals

❑ SaO2 >90%–92%

❑ CVP 8–12 mmHg

❑ MAP >65–70 mmHg

❑ PCWP 12–15 mmHg

❑ CI >2.1 L/min/m2

❑ Hemoglobin >7–9 g/dL

❑ Lactate <2.2 mM/L

❑ Urine output >0.5 mL/kg/h

Identify the cause

History of significant bleeding
or direct trauma to the
thoracic cavity?

YES, then consider cardiac injury,
cardiac tamponade, tension pneumothorax,
or hemorrhagic shock

NO, then proceed to the next question

Evidence of gastrointestinal hemorrhage,
vomiting, diarrhea?

YES, then consider and manage as
hypovolemic shock

NO, then proceed to the next question

Presence of fever
or hypothermia?

YES, then consider and manage as
septic shock

NO, then proceed to the next question

Presence of chest pain and/or
ischemic findings on ECG
with coronary risk factors?

YES, then consider and manage as
cardiogenic shock

NO, then proceed to the next question

Presence of
unexplained
bradycardia?

YES, then consider negative inotropic agents,
adrenal insufficiency, or hypothyroidism

NO, then proceed to the next question

Presence of
unexplained
hypoxemia?

YES, then consider and manage as
acute pulmonary embolism

NO, then proceed to the next question

Presence of abdominal pain or
low back pain?

YES, then consider intra-abdominal etiologies
and surgical consultation

NO, then proceed to the next question

Presence of wheezing with hives
or skin flushing?

YES, then consider and manage as
anaphylactic shock

NO, then proceed to
complete diagnostic approach below

Complete Diagnostic Approach

Complete Diagnostic Approach

History

Review all medications

Antihypertensives can cause significant hypotension, especially in the setting of volume depletion or over-diuresis.
Anaphylaxis should be considered if the patient recently started on a new drug and presented with respiratory distress.

Findings suggestive of hypovolemic shock

Findings suggestive of cardiogenic shock

Findings suggestive of distributive shock

Physical Examination

Vital signs

Temperature

Fever may suggest sepsis or anaphylactic reaction related to transfusion.
Hypothermia may be associated with sepsis, adrenal crisis, or myxedema.

Pulse

Bradycardia or tachycardia can either be a primary or secondary process.
Pulsus paradoxus may be seen in cardiac tamponade, pulmonary embolism, hemorrhagic shock, or tension pneumothorax.
Pulsus alternans may be seen in heart failure, severe aortic insufficiency, or hypovolemic shock.

Respiration

Tachypnea commonly occurs in pneumothorax, sepsis, and cardiogenic shock.
Hypopnea may be seen in narcotic or sedative overdose.

Blood pressure

Confirm arterial hypotension by checking blood pressure in both arms manually. Arterial line may be considered.
Postural hypotension suggests volume depletion or autonomic dysfunction. Do not test orthostatic hypotension in hypotensive patients.

Mental status

Altered mental status may indicate inadequate perfusion to vital organs or use of sedatives or narcotics.

Cutaneous

Decreased skin turgor and dry mucous membrane signify dehydration.
Cool extremities, clammy and mottled skin, peripheral cyanosis, and delayed capillary refill are commonly noted in cardiogenic shock and hypovolemic shock, whereas warm and moist skin may represent hyperdynamic phase of septic shock.
Extensive burns and severe trauma may be evident on inspection and are associated with significant fluid loss.
Hyperpigmentation may be an indicator of adrenal crisis.

Neck

Elevated jugular venous pressure (JVP) correlates with increased left ventricular end diastolic pressure (LVEDP) and decreased left ventricular ejection fraction (LVEF). Jugular venous distention or elevated JVP typically occurs in:

Kussmaul’s sign

Abdominojugular reflux (a positive abdominojugular reflux correlates with a PCWP of 15 mmHg or greater)

Cardiac tamponade
Constrictive pericarditis
Tricuspid insufficiency
Inferior vena cava obstruction
Heart failure (except for pure backward left-sided heart failure)

Jugular venous pressure waveform

Blunted y descent suggests cardiac tamponade or tricuspid stenosis.
Steep y descent suggests constrictive pericarditis or severe tricuspid insufficiency.

Cardiovascular

Decrescendo early systolic murmur

Acute severe mitral regurgitation

Third heart sound (S₃)

Heart failure

Pansystolic murmur along lower left sternal border with palpable thrill

Ventricular septal defect

Pericardial friction rubs

Pericarditis

Distant, muffled heart sounds

Cardiac tamponade

Pulmonary

Tracheal deviation

Tension pneumothorax

Stridor and wheezing

Rales

Chest percussion may aid in the diagnosis of tension pneumothorax, pleural effusions, and pneumonia

Abdominal

Grey Turner’s sign

Cullen’s sign

Hepatomegaly

Rebound tenderness with absent bowel sounds

Pulsatile mass

Abdominal aortic aneurysm

Rectal

Bright red blood or melena

Gastrointestinal hemorrhage

Diminished sphincter tone

Spinal cord injury

Extremities

Digital clubbing

Heart failure

Edema

Heart failure

Erythema at the site of venous access

Catheter-associated infection

Pelvic girdle pain or instability

Pelvic fracture

Genitals

Perform a pelvic examination in women of childbearing age to rule out ectopic pregnancy or pelvic inflammatory disease.

Neurologic

Agitation or delirium

Poor cerebral perfusion

Meningeal signs (nuchal rigidity, Brudzinski’s sign, and Kernig’s sign

Meningitis

Laboratory Findings

Complete blood count

In acute blood loss, hemoglobin and hematocrit levels may remain normal until volume repletion.
Leukocytosis with or without a left shift of neutrophils suggests sepsis.
Thrombocytopenia with alterations in coagulation panel indicates disseminated intravascular coagulation (DIC), which may be a complication of sepsis.

Electrolytes

Decreased bicarbonate levels may be the primary deficit in metabolic acidosis or the compensatory change in respiratory alkalosis.
Hyperkalemia due to transcellular shift is commonly associated with metabolic acidosis.

Coagulation panel (PT, PTT, INR, etc.)

Abnormalities in coagulation panel may be caused by disseminated intravascular coagulation (DIC), over-anticoagulation, or hepatic failure.

Cardiac markers

Check troponin and CK-MB levels when suspecting myocardial infarction.
Elevation in cardiac markers may be associated with both cardiac and extracardiac etiologies.

Liver function

Increased levels of conjugated bilirubin, alkaline phosphatase, and hepatic aminotransferases are typically seen in ischemic hepatitis (“shock liver”) due to cardiogenic shock.

Renal function

Prerenal azotemia and/or acute tubular necrosis may be associated with conditions of hypovolemia or reduced cardiac output.
Oliguria (urine output <0.5 mL/kg/h) is usually evident.

Lactate

Hyperlactatemia generally reflects the development of anaerobic metabolism in hypoperfused tissue and/or imparied hepatic clearance.
Lactate level could decrease within hours with effective therapy.^[1]

Arterial blood gas

Lactic acidosis may be an indicator of tissue hypoperfusion typically seen in septic shock.
Combined acid-base disorders are fequently encountered in different stages of shock.
Severe acidosis could blunt the effectiveness of vasopressors and potentiate the development of arrhythmias.

Cultures

Samples of blood, urine, and/or sputum should be sent for culture before administering antibiotics if sepsis is concerned.

Nasogastric aspirate

A negative nasogastric aspirate does not rule out upper gastrointestinal bleeding.

Pregnancy test

A pregnancy test should be performed on hypotensive women of childbearing age presenting with lower abdominal pain.

ECG Findings

ST segment elevation or depression, pathologic Q waves, hyperacute or negative T waves

Myocardial infarction or ischemia

Sinus tachycardia with S1Q3T3 pattern

Acute pulmonary embolism

Low QRS voltage with electrical alternans

Cardiac tamponade

QS deflections in precordial leads with right axis deviation and low QRS voltage

Pneumothorax

Bradyarrhythmias or tachyarrhythmias

Radiographic Findings

Chest radiograph may aid in establishing diagnosis in the following conditions:

Aortic dissection
Cardiac tamponade
Pneumonia complicating septic shock
Pulmonary edema complicating cardiogenic shock
Tension pneumothorax

CT scan may aid in directing management in the following conditions:

Hemodynamic Profiles and Echocardiography Findings

Type of Shock	Etiology	CO	SVR	PCWP	CVP	SVO2	Echocardiographic Findings
Cardiogenic	Acute Ventricular Septal Defect	↓↓	↑	N — ↑	↑↑	↑ — ↑↑	Large ventricles with poor contractility
	Acute Mitral Regurgitation	↓↓	↑	↑↑	↑ — ↑↑	↓
	Myocardial Dysfunction	↓↓	↑	↑↑	↑↑	↓
	RV Infarction	↓↓	↑	N — ↓	↑↑	↓	Dilated RV, small LV, abnormal wall motions
Obstructive	Pulmonary Embolism	↓↓	↑	N — ↓	↑↑	↓	Dilated RV, small LV
Obstructive	Cardiac Tamponade	↓ — ↓↓	↑	↑↑	↑↑	↓	Pericardial effusion, small ventricles, dilated inferior vena cava
Distributive	Septic Shock	N — ↑↑	↓ — ↓↓	N — ↓	N — ↓	↑ — ↑↑	Normal cardiac chambers with preserved contractility
Distributive	Anaphylactic Shock	N — ↑↑	↓ — ↓↓	N — ↓	N — ↓	↑ — ↑↑	Normal cardiac chambers with preserved contractility
Hypovolemic	Volume Depletion	↓↓	↑	↓↓	↓↓	↓	Small cardiac chambers with normal or high contractility

Treatment

Treatment

Management of shock consists of stabilization of the hemodynamic status and correction of the underlying cause once it is identified.

Cardiogenic shock

Obstructive shock

Distributive shock

Hypovolemic shock

Do’s

Do’s

Initial Management

Resuscitation should be initiated while investigation is ongoing. Correct the cause of shock immediately once it is identified.
The VIP (Ventilate-Infuse-Pump) approach is useful for ensuring an orderly sequence of therapeutic-diagnostic maneuvers.^[3]

Ventilate

Endotracheal intubation should be performed in patients with severe dyspnea, hypoxemia, or persistent or worsening acidemia (pH <7.30).

Infuse

A central venous catheter should be placed for the infusion of fluids and vasoactive agents and to guide fluid therapy.
A pulmonary artery catheter should be inserted for monitoring of blood pressure and blood sampling unless shock is rapidly reversed. (Indications)
An infusion of 300–500 ml of crystalloid fluid is usually administered during a period of 20–30 minutes.
End point of fluid therapy can be defined as a central venous pressure (CVP) of a few millimeters of mercury (mmHg) above the baseline to prevent fluid overload.^[4]

Pump

Vasopressors are indicated in hypotension that is severe or refractory to fluid challenge.
Norepinephrine (0.1–2.0 μg/kg/min IV) is the first choice of vasopressor, while epinephrine (0.1–0.5 μg/kg/min IV) is reserved for severe hypotension as the second-line agent.
Isoproterenol (0.5–5.0 μg/min IV) should be limited to the treatment of hypotensive patients with severe bradycardia.
Adjunctive vasopressin (0.01–0.04 U/min IV) to norepinephrine should be considered only in hyperdynamic phase of distributive shock.

Don’ts

Don’ts

Do not test orthostatic hypotension in hypotensive patients.
Do not rely solely on SpO2 readings from pulse oximeter. SaO2 from blood gas analysis provides more precise status of oxygenation.
Do not administer low-dose dopamine (<5 μg/kg/min) to preserve renal function in patients with shock.

References

References

↑ ^1.0 ^1.1 Vincent, JL.; De Backer, D. (2013). “Circulatory shock”. N Engl J Med. 369 (18): 1726–34. doi:10.1056/NEJMra1208943. PMID 24171518. Unknown parameter |month= ignored (help)
↑ Rosen, Peter; Marx, John A. (2013). Rosen’s emergency medicine : concepts and clinical practic. Philadelphia, PA: Elsevier/Saunders. ISBN 978-1-4557-0605-1.
↑ Weil, MH.; Shubin, H. (1969). “The VIP approach to the bedside management of shock”. JAMA. 207 (2): 337–40. PMID 5818156. Unknown parameter |month= ignored (help)
↑ Dellinger, RP.; Levy, MM.; Rhodes, A.; Annane, D.; Gerlach, H.; Opal, SM.; Sevransky, JE.; Sprung, CL.; Douglas, IS. (2013). “Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012”. Crit Care Med. 41 (2): 580–637. doi:10.1097/CCM.0b013e31827e83af. PMID 23353941. Unknown parameter |month= ignored (help)

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Zaghw, MBChB. [2]