Shock resident survival guide

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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]; Associate Editor(s)-in-Chief: Ahmed Zaghw, MBChB. [2]

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) indicative of tissue hypoperfusion.[1] Management of shock consists of stabilization of the hemodynamic status and correction of the underlying cause.

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.

Abbreviations: MAP, mean arterial pressure; SBP, systolic blood pressure.

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

Arterial hypotension

SBP <90 mm Hg or
MAP <70 mm Hg

+ Any sign of hypoperfusion

Altered mental status
Cold, clammy skin
Oliguria
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
YES
 
 
 
 
 
 
 
 
 
 
NO
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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 (Indications)

❑ ± Cultures of blood, urine, etc.

❑ ± Pulmonary artery catheter (Indications)

❑ ± Echocardiography
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Immediate Goals

❑ 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.

Accompanying symptoms that could pinpoint the underlying disease include:

Abdominal pain
Chest discomfort
Diarrhea
Dyspnea
Hematemesis
Hematochezia
Polydipsia
Polyuria
Vomiting
 
 
 
 
 
 

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 JVP
Heart failure
Tricuspid stenosis
Pulmonary hypertension
Superior vena cava obstruction
Constrictive pericarditis
Cardiac tamponade
Kussmaul's sign
Constrictive pericarditis
Restrictive cardiomyopathy
Tricuspid stenosis
Superior vena cava obstruction
Right ventricular infarction
Abdominojugular reflux
❑ 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)
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
Anaphylaxis
Acute exacerbation of chronic obstructive pulmonary disease
Rales
Anaphylaxis
Pneumonia
Heart failure
Chest percussion may aid in the diagnosis of tension pneumothorax, pleural effusions, and pneumonia

Abdominal

Grey Turner's sign
Acute pancreatitis
Blunt abdominal trauma
Retroperitoneal hemorrhage
Ruptured abdominal aortic aneurysm
Ruptured ectopic pregnancy
Cullen's sign
Acute pancreatitis
Blunt abdominal trauma
Ruptured abdominal aortic aneurysm
Ruptured ectopic pregnancy
Hepatomegaly
Inferior vena cava obstruction
Heart failure
Rebound tenderness with absent bowel sounds
Sepsis due to Intraabdominal infection
Ischemic colitis
Gastrointestinal hemorrhage
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
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:

Occult internal hemorrhage
Pulmonary embolism
 
 
 
 
 
 

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

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

  • 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
  • Infuse
  • Pump

Don'ts

References

  1. 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)
  2. 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. 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)