2. OBJECTIVES
To develop an understanding of the definition and
Pathophysiology and Stages of shock.
To develop an understanding and overview of the
different types of shock.
To discuss Management of different Types of Shock.
4. Definition of Shock
Oxygen delivery ≠ Oxygen Consumption
(DO2 ≠ VO2)
“A state of cellular and tissue hypoxia
due to Reduced oxygen delivery
and/or Increased oxygen consumption
or Inadequate oxygen utilization”
O2 Consumption O2 Delivery
Empirical Criteria for Diagnosis of
Circulatory Shock
Systemic Arterial Hypotension
(SBP <90 mm Hg/ MAP <65 mmHg
associated tachycardia)
Clinical Signs of Tissue Hypoperfusion
(Cutaneous, Renal, Neurologic)
Hyperlactatemia
(Abnormal Cellular Oxygen Metabolism)
5. Understanding of Shock
Physiology
The major physiologic determinants of tissue perfusion (and systemic blood
pressure [BP]) are
Cardiac output (CO) and
Systemic Vascular resistance (SVR)
BP = CO X SVR
CO is the product of heart rate (HR) and stroke volume (SV):
CO = HR X SV
Biologic processes that change any one of these physiologic parameters can result
in hypotension and shock.
6. Understanding Shock-SVR
SVR regulated by Vessel length, Blood viscosity, blood vessel
Diameter/tone.
Dilatation opens blood vessels and increases volume
to area but decreases return to heart
Constriction decreases volume to area but
increases return to heart
7. Understanding Shock-Stroke Volume
Volume of blood pumped by the heart in one Cycle
What affect stroke volume ?
Blood volume
Rhythm problems
Heart muscle problem
Mechanical obstruction
8. Understanding of Shock
Tissue perfusion is driven by Blood Pressure!
So….
In other words
When the blood flow (pressure) and O2 delivery to the cell are too low
There will be shock!!!!
9. Why should you care Shock?
High mortality 20%-90%
O2 Deprivation and Build Up of waste products
Could be fatal without timely management
Rapidly become Irreversible>>>Multiorgan failure (MOF)>>>Death
The early stages of shock are more amenable to therapy and are more likely
to be reversible
Early , timely and appropriate management
-Deterioration can be prevented
-Signs of impending deterioration can be reversed
-Reduces mortality
13. Types and Etiology of Shock
• Pulmonary
vascular
• Mechanical
• Septic Shock
• Non-septic
• Cardiomyopathic
• Arrythmogenic
• Mechanical
• Hemorrhagic
• Non-Hemorrhagic
Hypovolemic
Shock
Cardiogenic
Shock
Obstructive
Shock
Distributive
Shock
COMBINED
SHOCK
Example:
Sepsis/Pancreatiti
s + Hypovolemic +
Cardiogenic shock
Severe Traumatic
Injury>>Hypovole
mic + Distributive
14. Epidemiology of Shock
62%
16%
16%
4% 2%
In a Trial of 1600 Patients in ICU
Distributive(Septic) 62%
Hypovolemic 16%
Cardiogenic 16%
Obstructive 4%
Other Distributive Shock 2%
34%
34%
30%
2%
Study of 103 Patients in a busy
Urban ED
Septic Shock 33%
Hypovolemic 33%
Cardiogenic 29%
Other forms of Shock 2%
15. EVALUATIONS OF SHOCK
Resuscitation should be started even while investigation of the cause is ongoing
Once identified, the cause must be corrected rapidly
Undifferentiated Shock!!!!
Medical History
Physical Examination-ABCDEFG,SAMPLE
Clinical Investigations
16.
17. Initial Treatment Approach to Shock
Key Principles in the Treatment of Shock
1. Recognize shock early
2. Assess for type of shock present
3. Initiate therapy simultaneous with the evaluation into the etiology of shock
4. Restoration of oxygen delivery is the aim of therapy
5. Identify etiologies of shock which require additional lifesaving interventions
18. Initial Approach to all types of Shock
❑ Early, adequate hemodynamic support of patients in shock is crucial
❑ The initial management of shock is problem-oriented, and the goals are therefore
the same, regardless of the cause
Important components of resuscitation is The VIP rule
VENTILATE
INFUSE
PUMP
• O2 Administration
• Fluids Administration
• Vasoactive Drug
administration
19. The Initial management of shock
A
• Establish A Patent Airway
• Basic Airway Manure
• Intubation/MV
B
• Administration of oxygen
• To increase oxygen delivery
and prevent pulmonary
hypertension
C
• Fluids Resuscitation(Type,
Rate and Objective of Fluids)
• Vasoactive Agents
(Vasopressors, Inotropic
Agents, Vasodilators)
• Mechanical Support
(IABP,ECMO)
TYPE OF FLUID>> CRYSTALLOIDS, COLLOIDS
RATE OF FLUID>>300-500ML OVER 20-30 MINS
OBJECTIVE OF FLUID ADMINISTRATION>>INCREASE SYSTEMIC
ART PRESSURE>>HR>>UOP
20. Prognosis
Sepsis and septic shock
Are associated with long-term morbidity and mortality
Requiring placement into long-term acute care facilities or post-acute care centers.
Septic shock has a mortality rate between 40% and 50%.
Cardiogenic shock
Mortality rate ranging from 50% to 75%, an improvement over prior mortality rates.
Hypovolemic and obstructive shock
Generally have much lower mortality and respond better to timely treatment.
21. 68 Years of Male with History of HTN and Duodenal Ulcer
presents to the ER with epigastric abdominal pain with
radiation to his back and dizziness. The patient is hypotensive,
tachycardic, Afebrile, and with cool and clammy skin
What type of Shock is this?
22. Hypovolemic Shock
Due to reduced intravascular volume (i.e., reduced preload), which, in turn, reduces
CO
Non-hemorrhagic
Hemorrhagic
23. Hypovolemic Shock-Causes
Non-hemorrhagic
Gastrointestinal losses
Skin losses
Renal losses
Third space losses into the extra vascular space
Hemorrhagic
Trauma
Gastrointestinal bleeding
Intraoperative and postoperative bleeding
Retroperitoneal bleeding
Tumor or abscess erosion into major vessels
Ruptured ectopic pregnancy, postpartum hemorrhage, uterine or vaginal hemorrhage
24. CLASSIFICATION OF HEMORRHAGIC SHOCK
In a normal Adult, a tachycardia after blood loss indicates at least a 15%
loss of blood volume(<750 MLs)
CLASS PULSE B.P CNS STATUS URINE
OUTPUT
BLOOD LOSS FLUID
REPLACEMEN
T
CLASS I <100 BPM NORMAL SLIGHTLY
ANXIOUS
>30ML/HR <15%
750CC
CRYSTALLOID
S
CLASS II >100 BPM NORMAL MILDLY
ANXIOUS
15-20ML/HR 15%-30%
750-1500 CC
CRYSTALLOID
S
CLASS III >120 BPM DECREASED CONFUSED 5-15 ML/HR 30%-40%
1500-2500 CC
CRYSTALLOID
S+BLOOD
CLASS IV >140 BPM DECREASED LETHARGIC NIL 40%
>2500 CC
CRYSTALLOID
S+BLOOD
25. Hypovolemic Shock-Management
Maximize oxygen delivery Control further blood loss Fluid resuscitation
Adequate Ventilation, Increase O2
saturation of Blood and Restoring
Blood Flow
-Assess Airway and Breathing
-High Flow O2/ Ventilatory Support
-IPPV
-Two large-bore IV lines/EJV/CVC/IO
-Arterial line (ABP,ABG)
-Initial fluid resuscitation
-Crystalloids-RL/NS (1-2 L)
-Type O blood
-Position
Both crystalloid and type O blood
(Marked Hypotension, Class IV Bleed)
Trauma
External bleeding should be controlled
with direct pressure
Internal bleeding-surgical
Long-bone fractures -Traction to
decrease blood loss.
GI Bleed
PPI
Vasopressin/ Octriotide infusion
Endoscopy, Sengstaken-Blakemore
tube
Gynecological bleeding
Surgical intervention.
Crystalloids Vs colloids (?? Best for
resuscitation)
26. A 55 YO/M with HTN,DM presents in ED with “Crushing”
substernal chest pain, diaphoresis, hypotension, tachycardia
and cool, clammy extremities.
What Type of Shock is This?
27. Cardiogenic Shock
Clinical Definition of Cardiogenic Shock is “Decreased cardiac output and
evidence of tissue hypoxia in the presence of adequate intravascular
volume”
28. Persistent (>30 minutes) Hypotension with systolic arterial pressure <90mm Hg
Signs and symptoms of end organ hypoperfusion
(Restlessness, Confusion, cold cyanotic extremities, oliguria<30ml/hr)
Reduction in cardiac index <2.2 litres /min/m2
Presence of elevated left ventricle filling pressure(PCWP>18 mm Hg)
Cardiogenic Shock criteria
29. Cardiogenic Shock-Causes
….
Cardiomyopathic Mechanical Arrythmogenic
Myocardial infarction Severe valvular insufficiency Tachyarrhythmia
Severe right ventricle
infarction
Acute valvular rupture Bradyarrhythmia
Myocarditis, Myocardial
contusion
Acute or severe ventricular
septal wall defect
Acute exacerbation of severe
heart failure from dilated
cardiomyopathy
,
Ruptured ventricular wall
aneurysm
30. Cardiogenic Shock-Investigation
ECG
Chest X-ray
Echocardiography
ABG, Lactate, Electrolytes, Cardiac enzymes, Renal parameters
Right heart catheter
(to measure cardiac output, central venous, pulmonary artery and wedge pressures and mixed
venous blood)
Urinary catheter(measure hourly urine output)
31. Cardiogenic Shock-Management
1.LIFE SAVING INTERVENTIONS
Emergency revascularization: either PCI (if coronary anatomy amenable) or CABG (if coronary anatomy
not amenable to PCI) in MI
Peri-interventional antiplatelet and antithrombotic medication
CS due to mechanical complications: Urgent Interventional surgical Closure
CS due to Arrythmogenic: Correct Arrhythmia
2.PHARMACOLOGIC CIRCULATORY SUPPORT
Fluid administration
Vasoactive agents (Vasopressors and Inotropic support)
32. Cardiogenic Shock-Management
3.MECHANICAL CIRCULATORY SUPPORT (MCS)
Percutaneous short-term MCS devices (IABP, TandemHeart and Impella CP,ECMO)
Surgical mechanical circulatory support devices and heart transplantation
33.
34.
35. DISTRIBUTIVE SHOCK
Vasodialatory shock“
Caused by Loss of Vasomotor Control
resulting in arteriolar/venular dilation.
Characterized by severe peripheral
vasodilation and low SVR
Systemic vasodilation leads to decreased
blood flow to the brain, heart, and kidneys
causing damage to vital organs
36. 81 Y/F presents in ED with Chest infection and altered mental
status. She is febrile to 39.4, hypotensive with a widened
pulse pressure, tachycardic and with warm extremities.
What Type of Shock is This?
37. Septic Shock
Sepsis
Two or more of SIRS criteria
• Temp > 38 or < 36 C
• HR > 90 • RR > 20
• WBC > 12,000 or < 4,000
• Plus the presumed existence of infection
• Blood pressure can be normal!
Sepsis,Severe Sepsis and Septic Shock
• Sepsis: Systemic host response to infection with SIRS
• Severe Sepsis: Sepsis plus end-organ dysfunction or hypo perfusion
• Septic Shock: Sepsis with hypotension, despite fluid resuscitation; evidence
of inadequate tissue perfusion
40. Septic Shock-Treatment
Antibiotics- Survival correlates with how quickly the correct
drug was given
Cover gram positive and gram negative bacteria
Add additional coverage as indicated
Pseudomonas- Gentamicin or Cefepime
MRSA- Vancomycin
Intra-abdominal or head/neck anaerobic infections-
Clindamycin or Metronidazole
Asplenic- Ceftriaxone for N. meningitidis, H. infuenzae
Neutropenic – Cefepime or Imipenem
41. A 34 YO/F presents to ER after dining at a restaurant,where
shortly after eating the first few bites of her meal, became
anxious, diaphoretic, began wheezing, noted diffuse pruritic rash,
nausea, and a sensation of her “throat closing off”. She is
currently hypotensive, tachycardic and ill appearing with
Dyspnea.
What Type of Shock is This?
42. Anaphylactic Shock
Anaphylaxis is a Rapid, Generalized often unanticipated,
immunologically mediated events
that occur after exposure to certain foreign substance.
Causes:
Foods (Milk, soy, eggs, nuts, and shellfish)
Medications (Antibiotics [penicillin], NSAIDs, Anesthetics)
Venom (Hymenoptera stings)
Intravenous contrast materials, and latex.
Idiopathic-Up to 20%
46. Anaphylactic Shock-Treatments
Airway Breathing Circulation
Disability Exposure
ECG, Cardiac /Hemodynamic Monitoring, Pulse
Oxymetry, IV Cannulations
Establish Patent Airway
High Flow O2,
IV Fluids Challenge
Medications
Consider Early Intubation/Surgical
Airway
Consider Epinephrine Infusion if
Shock
47. Anaphylactic Shock-Treatments
Epinephrine
0.3 mg IM of 1:1000 (Epi-pen)
Anterolateral Thigh
Repeat every 5-15 min as needed
Caution with patients taking beta blockers
IV Fluid Challenge
1-2 L in First Hour
48. Anaphylactic Shock-Treatments
Corticosteroids
Methylprednisolone 1-2 mg /KG IV /Prednisone 0.5-1 mg/KG PO
Antihistamines
H1 blocker- Diphenhydramine 25-50 mg IV/IM/PO
H2 blocker- Ranitidine 50 mg IV/IM,150MG PO
Severe Wheeze/Dyspnea
Sabutamol 5 MG X 3 Doses in an hour
Atrovent nebulizer
Magnesium sulfate 2 g IV over 20 minutes
49. A 41 YO/M Presents to ER after a car accident, Complaining of
decreased sensation below his waist and is now hypotensive,
bradycardic, with warm extremities
What Type of Shock is This?
50. Neurogenic Shock
“Vasogenic shock”
▪ Associated with cervical and high thoracic spine injury
▪ Primary spinal cord SCI occurs within minutes
and Secondary SCI occurs hours to days
after the initial insult
▪ A Combination of both primary and secondary injury
that lead to loss of sympathetic tone and
thus unopposed parasympathetic response
driven by the Vagus nerve
▪ Leads to decreased tissue perfusion and initiation of the shock response.
Hypotension, Brady arrhythmia, and Temperature dysregulation/flushed warm skin
51. Neurogenic Shock/Treatment
A,B,C ---Remember C-spine precautions
Fluid resuscitation
❑ The first-line treatment for hypotension is intravenous fluid resuscitation
❑ If hypotension persists despite euvolemia, vasopressors and inotropes are the
Second lines.
❑ Proffered agent Norepinephrine (Hypotension and Bradycardia)
❑ Recommend MAP at 85–90 mmHg for the first 7 days(Improve spinal cord
perfusion)
❑ For Bradycardia: Atropine, Pacemaker
❑ Methylprednisolone is controversial & given early and in high doses
❑ Initial c-spine immobilization is important to prevent further spinal cord injury.
(Miami J/Philadelphia collar)
❑ Surgical intervention may be required for decompression of spinal injury
52. Obstructive Shock
Obstructive shock is mostly due to extracardiac causes of cardiac pump failure and often
associated with poor right ventricle output.
Associated with a physical Obstruction/blockage of
Great Vessels or something interfering with filling/
Emptying of heart
The causes can be divided into two categories
1.Pulmonary vascular 2.Mechanical
Most Common Causes
Cardiac Tamponade
Pulmonary Embolism
Tension Pneumothorax
53. Obstructive Shock/Cardiac Tamponade
A Clinical syndrome caused by the accumulation of fluid in the pericardial space
Prevents venous return to and contraction of heart
Reduced Ventricular filling and Cardiac Compromise
“Clinical diagnosis” , Large Heart CXR, 2D-Echo,
“Beck’s Triad” Classic Symptoms
“Definitive Therapy”
Emergency subxiphoid percutaneous drainage
Pericardiocentesis (with or without echocardiography guidance)
55. Obstructive Shock/Pulmonary Embolism
Thrombus Vs Embolus
“Sudden lodgment of a blood clot in a Pulmonary Artery
With subsequent obstruction of blood supply to
the Lung parenchyma”
Unable to generate enough pressure to overcome
the high pulmonary vascular resistance with PE
Right Ventricular Failure
57. PE-Signs and Symptoms
Classic Symptoms
Sudden, unexplained Dyspnea(SOB)
Dull Chest Pain (Pleuritic, worse with a deep breath)
Cough.
Classic Signs
Tachycardia, Tachypnea, Decreased breath sounds over a portion of a lung
Rales/Crackles
Hypotension
Elevated Pressure in the Neck veins, suggesting an obstruction in the pulmonary
artery
Swelling /tenderness over the thigh or calf
58. PE - Diagnosis
ABG-Severe Hypoxemia
Unstable>>>CT Chest PE
Stable>>>Well’s Criteria, D-Dimer
Well’s Score ≤4>>>D-Dimer(+)>>>CT PE
Well’s Score 5/6>>>CT PE/VQ Scan
Well’s Score ≥ 7>>> Begin anticoagulation without delay
Rx: Heparin, Consider Thrombolytics
59. Tension Pneumothorax
Air trapped in pleural space with 1-way Valve
Air/pressure builds up
Mediastinum shifted
Obstructs venous return to Heart
No Tests!!!! Classic Symptoms
Hypotension
Jugular Vein Distention
Diminished or Absent Breath Sounds
Tracheal Deviation
62. Pearls
Shock is a clinical manifestation of Circulatory failure
Associated with High morbidity and Mortality.
Four types of shock: Distributive, Cardiogenic, Hypovolemic, and Obstructive.
Requires a good understanding of underlying Pathophysiology, clinical,
biochemical, and hemodynamic manifestations of the different types of shock.
Serum lactate level is a useful risk stratification tool in managing
undifferentiated shock.
Timely diagnosis and initiation of appropriate therapy are of paramount
importance. (Prevent Progression to Irreversible MOF and Death)
Treatment includes Hemodynamic stabilization and Correction of underlying
etiology of shock.
63. Pearls Prognosis and Patient Education
Patient Education is important about
What is Shock?
What are the Symptoms of Shock?
Should I see a Doctor or Nurse?
Will I Need Tests?
How is Shock Treated?
64. References
1.National Center for Biotechnology Information (NCBI)
www.ncbi.nlm.nih.gov/books/NBK531492/
2.Wolters Kluwer Health- UpToDate for Clinicians and Medical Students
www.uptodate.com/contents/definition-classification-etiology-and-
Pathophysiology-of-shock-in-adults?
3.Jean-Louis Vincent, M.D.,Ph.D and Daniel De Backer, M.D., PhD, New England
Journal of Medicine, https://www.nejm.org/doi/full/10.1056/nejmra1208943
4. European Heart Journal, Volume 36, Issue 20, 21 May 2015, Pages 1223–
1230,https://doi.org/10.1093/eurheartj/ehv051