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| Shock Resident Survival Guide |
|---|
| Overview |
| Causes |
| FIRE |
| Diagnosis |
| Do's |
| Don'ts |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Shock is the syndrome of circulatory failure that results in inadequate cellular oxygen utilization. The diagnosis of shock is based on clinical signs and biochemical abnormalities indicative of tissue hypoperfusion.[1]
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
A Focused Initial Rapid Evaluation (FIRE) should be performed to identify patients in need of immediate intervention.
Boxes in the salmon color signify that an urgent management is needed.
Identify cardinal findings that increase the pretest probability of shock
❑ SBP <90 mmHg or ❑ MAP <70 mmHg ❑ Cold, clammy skin ❑ Oliguria | |||||||||||||||||||||||||||||||||||||||||||||
YES | NO | ||||||||||||||||||||||||||||||||||||||||||||
Ventilate—Infuse—Pump (VIP) ❑ Oxygen ± mechanical ventilation ❑ Normal saline 300–500 mL over 20–30 min ❑ ± Norepinephrine 0.1–2.0 μg/kg/min | Consider other causes (eg, chronic hypotension, syncope) | ||||||||||||||||||||||||||||||||||||||||||||
❑ ECG monitor ❑ Pulse oximeter ❑ Arterial blood gas ❑ Central venous catheter ❑ CBC/DC/SMA-7/LFT/PT/PTT/INR ❑ Troponin, CK-MB ❑ Lactate ❑ Chest radiograph ❑ Foley catheter ❑ ICU admission ❑ ± Transfusion ❑ ± Cultures of blood, urine, etc. ❑ ± Pulmonary artery catheter ❑ ± Echocardiography | |||||||||||||||||||||||||||||||||||||||||||||
❑ SaO2 >90%–92% ❑ CVP 8–12 mmHg ❑ MAP >65–70 mmHg ❑ PCWP 12–15 mmHg ❑ CI >2.1 L/min/m2 ❑ MVO2 >60% ❑ SCVO2 >70% ❑ Hemoglobin >7–9 g/dL ❑ Lactate <2.2 mM/L ❑ Urine output >0.5 mL/kg/h | |||||||||||||||||||||||||||||||||||||||||||||
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:
- A positive abdominojugular reflux correlates with a PCWP of 15 mmHg or greater and may be seen in:
- Cardiac tamponade
- Constrictive pericarditis
- Tricuspid insufficiency
- Inferior vena cava obstruction
- Heart failure (except for pure backward left-sided heart failure)
-
- Blunted y descent suggests cardiac tamponade or tricuspid stenosis.
- Steep y descent suggests constrictive pericarditis or severe tricuspid insufficiency.
- Cardiovascular
- Pulmonary
-
- Chest percussion may aid in the diagnosis of tension pneumothorax, pleural effusions, and pneumonia
- Abdominal
- Rectal
- Extremities
-
- Erythema at the site of venous access
- Genitals
- Perform a pelvic examination in women of childbearing age to rule out ectopic pregnancy or pelvic inflammatory disease.
- Neurologic
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
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 | 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 |
| Cardiac Tamponade | ↓ — ↓↓ | ↑ | ↑↑ | ↑↑ | ↓ | Pericardial effusion, small ventricles, dilated inferior vena cava | |
| Distributive | Septic Shock | N — ↑↑ | ↓ — ↓↓ | N — ↓ | N — ↓ | ↑ — ↑↑ | Normal cardiac chambers with preserved contractility |
| Anaphylactic Shock | N — ↑↑ | ↓ — ↓↓ | N — ↓ | N — ↓ | ↑ — ↑↑ | ||
| Hypovolemic | Volume Depletion | ↓↓ | ↑ | ↓↓ | ↓↓ | ↓ | Small cardiac chambers with normal or high contractility |
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.[2]
- 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.
- 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.[3]
- 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
- 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
- ↑ 1.0 1.1 1.2 1.3 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) - ↑ 2.0 2.1 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) - ↑ 3.0 3.1 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) - ↑ Parrillo, Joseph E.; Ayres, Stephen M. (1984). Major issues in critical care medicine. Baltimore: William Wilkins. ISBN 0-683-06754-0.
- ↑ Weil, Max Harry; Shubin, Herbert (1967). Diagnosis and Treatment of Shock. Williams & Wilkins. ISBN 1125885874.