Shock concept and its management

1. FANS TRAINING COURSE
CIRCULATORY SHOCK
DWI KARTIKA RUKMI,SP.KEP.MB
6/20/21 FANS UNJANI YOGYAKARTA 0

2. Welcome to our
virtual classroom,
my dearstudents!
IN OUR CLASS, WE RESPECT EACH OTHER,
WE DO OUR BEST, AND WE SUPPORT ONE
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F A N S U N J A N I Y O G YA K A R TA
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3. CIRCULATORY SYSTEM
DEFINITION AND CLASSIFICATION
SHOCK
PATHOPYSIOLOGY AND PHYSIOLOGICAL COMPENSATORY MECHANISMS
CLINICAL PRESENTATION
MANAGEMENT OF SHOCKS
A
B
C
D
E
BRAIN INFOGRAPHIC

4. CIRCULATORY
SYSTEM
F A N S U N J A N I Y O G YA K A R TA
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Jones and Bartlett
Publisher

5. Shock is a clinical state in
which disparity of oxygen
supply and demand at cell
level results in tissue
hypoxia and incipient failure
of cell function
DEFINITION
HYPODINAMIC:
Hypovolemic, cardiogenic,
obstructive
HYPERDINAMIC:
Distributive (Sepsis,
anaphylactic, neurogenic)
CLASSIFICATION
Blood and fluid compartment
Vascular system
Circulatory system
Heart .
MAIN PHYSIOLOGYCAL
PARTS INVOLVED
A
B
C
SHOCK
It leads to distinctive
symptoms and signs,
initially of compensation
and later of failure.
Song & Soni, 2013
Song & Soni, 2013;
Kloner, 2020
Standl et al, 2018

6. SHOCK CLASSIFICATION
SHOCK
Hypovolemic shock is a condition care
emergency associated with significant
of intravascular volume resulting in
decreased preload, SV, and CO
(Moranville et al, 2011)
Cardiogenic shock is a severe life-
threatening condition of acute heart
failure and hypotension associated with
complex physiologic alterations (Kloner et
al, 2020)
.
Obstructive shock: occurs when there is
obstruction of blood flow from the heart
or great vessels. The main acute causes
are cardiac tamponade, massive
pulmonary embolus and tension
pneumothorax, although there are many
other rarer causes (Morgan, 2013)
.
Septic shock is the condition whereby sepsis
(infection that involves the blood) is associated
with hypotension. A life-threatening condition
that happens when your blood pressure drops
to a dangerously low level after an infection
(Kloner et al, 2020)
Neurogenic shock refers to reduced SVR
and hypotension which is most commonly
caused by spinal cord injuries at or above
the level of the sixth thoracic vertebrae.
(Damiani, 2018; Moranville et al, 2011)
Anaphylaxis is an immunoglobulin (IgE)-
mediated, rapid-onset systemic allergic
reaction . Anaphylaxis shock is form of severe
anaphylaxis (Moranville, 2011, Song & Soni,
2013)
HYPODINAMIC HYPERDINAMIC

7. SHOCK
CLASSIFICATIO
N Marketers must link the price
to the real and perceived
value of the product, but they
also must take into account.
STEP 01
Marketers must link the price
to the real and perceived
value of the product, but they
also must take into account.
STEP 02
Marketers must link the price
to the real and perceived
value of the product, but they
also must take into account.
STEP 03
Marketers must link the price
to the real and perceived
value of the product, but they
also must take into account.
STEP 04
Standl et al, 2018

8. 00
SHOCK
PATHOPHYSIOLOG
Y
Taha & Elbaih, 2017

9. 03
02
01
COMPENSATOR
Y
PHYSIOLOGICA
L RESPONSE
FAILURE OF
PHYSIOLOGICA
L RESPONSE
FINAL
RESULT
MULTI-ORGAN DYSFUNCTION
DEATH
Song & Soni, 2013

10. Invasive haemodynamic measurements
GENERAL SIGNS:
• TACHYCARDIA
• TACHYPNOEA
• CONFUSION
• OLIGURIA
Specific signs : Cold and clammy, Sweat,
Pale , Pinpoint pupils, Cyanosis
Causes : Major haemorrhage Perforated/
obstructed bowel, Burns ,Pancreatitis, Diabetic
ketoacidosis, Diabetes insipidus , Diarhea, Vomiting,
Excessive sweating
Common investigations : Full blood count, urea and
creatinine, electrolytes, clotting studies Arterial
blood gas and lactate, Chest X-ray,
Electrocardiogram
Specific investigations : Amylase, Supine and
erect, abdominal X-ray, CT of abdomen, Endoscopy
HYPOVOLEMIC SHOCK
INDICATOR VALUE
Cardiac index ⬇
Pulmonary artery occlusion pressure ⬇
Central venous pressure ⬇
Systemic vascular resistance ⬆
Oxygen delivery ⬇
Song & Soni, 2013; Shagana et al, 2018

11. Well function before MAP falls
below 50-60 mmHg.
CEREBRAL CIRCULATION
Maintain blood for heart and
brain first, then other organs 
failure
Increases minute volume but CO
still decreased so V/Q ratio
increased  respiratory failure
CARDIOVACULAR
AND
RESPIRATORY
Increasing Renin Production
 converts angiotensinogen
to angiotensin I 
angiotensin 2 in lung and liver
 vasoconstriction and
aldosterone production
RENAL
Increasing antidiuretic
hormone (ADH)
reabsorption of Na Cl and
water
NEUROENDOCRIN
E SYSTEM
HIPOVOLEMIC SHOCK EFFECTS
Shagana et al, 2018

12. HIPOVOLEMIC SHOCK TREATMENTS
Three Goals:
1. Fluid resuscitation
• Immediate intravascular volume replacement with balanced crystalloids (RL/Na Cl 0,9%)(B)  1 L in 10-15 minutes
• Wide bore peripheral venous access (A)  14 to 16 gauge
• For patients with large burns, the modified Brooke formula can give an indication of the volume replacement required in the first 24 h
2. Maximizing Oxygen Delivery
• To prevent or alleviate hypoxia, endotracheal intubation with normo-ventilation usually follows (A)
• Monitoring ABG, pH, Electrolyte serum is also necessary
• Intra aortic balloon for monitoring ventricular filling pressure
Standl et al, 2018,;Song & Soni,
2013; Haberal et al, 2010;

13. HIPOVOLEMIC SHOCK TREATMENTS
3. Control further blood loss
• The extent of blood loss can be roughly estimated using the ATLS (Advanced
Trauma Life Support) score (B).
• Transferred directly to a trauma center and surgical management should be
undertaken as soon as possible using the damage control surgery (DCS)
approach (B).
• Persisting hypotension, especially in patients with head trauma, should
administration of a vasoconstrictor(e.g., norepinephrine) to achieve a systolic
arterial pressure (SAP) ≥ 90 mmHg (B)  Dopamine, dobutamine,
norepinephrine to increase BP and CO.
• Transfusion: controllable bleeding  red cell concentrate (RCC) , uncontrolled
bleeding, irrespective of the current hemoglobin value, should receive
transfusions of RCC, fresh frozen plasma (FFP), and platelet concentrates (PC).
• Patients with traumatic or peripartum bleeding should also be given 1 to 2 g
tranexamic acid at an early stage (A).
• Multidisciplinary treatment includes early stabilization of coagulation by
of coagulation factors
Standl et al, 2018,;Song & Soni, 2013; Haberal et
al, 2010; Sphan et al, 2007

14. Invasive haemodynamic measurements
GENERAL SIGNS:
• TACHYCARDIA
• TACHYPNOEA
• CONFUSION
• OLIGURIA
Specific signs : S3 gallop, Basal inspiratory
crackles on chest auscultation
Causes : Myocardial infarction, Acute
valvular failure, Hyper/ hypothyroidism .
Common investigations : Full blood count, urea and
creatinine, electrolytes, clotting studies Arterial
blood gas and lactate, Chest X-ray,
Electrocardiogram
Specific investigations : Echocardiography
CARDIOGENIC SHOCK
INDICATOR VALUE
Cardiac index ⬇
Pulmonary artery occlusion pressure ⬆
Central venous pressure Normal or ⬆
Systemic vascular resistance ⬆
Oxygen delivery ⬇
Song & Soni, 2013; Shagana et al, 2018

15. CARDIOGENIC SHOCK MANAGEMENT
• Echocardiography and invasive monitoring are the pillars of diagnosis.
• The primary goal removing the cardiac causes of the shock: if there is acute coronary
(ACS) so reperfusion in ACS by means of percutaneous coronary intervention (PCI) with the
insertion of stents (bare metal stent, BMS; drug-eluting stent, DES) is a must (recommendation
grade: A).
• A surgical or other interventional treatment of mechanical causes and structural heart disease,
surgical or interventional ablation, and pacemaker therapy is other way.
• If hypovolemia is present, conservative boluses of crystalloids (250–500 mL) are reason- able
the patient is being stabilized for cardiac catheterization.
• Continuous pulse oximetry should be used to monitor for respiratory compromise  in the
care setting blood oxygen saturations of >90% are acceptable
• Symptomatic treatment is under- taken with the aim of improving end organ perfusion,
microcirculation, and cellular oxygen utilization  dobutamine (recommendation grade: B),
norepinephrine (recommendation grade: B), and epinephrine (recommendation grade: 0),
vasodilators (recommendation grade: 0), calcium sensitizers (recommendation grade: 0), PDE3
inhibitors (recommendation grade: 0), antiarrhythmic drugs, and more (Table 2), but also
mechanical circulatory support such as intra-aortic balloon counter-pulsation (recommendation
grade: B)
• When life-threatening changes in fluid, electrolyte, and acid-base balance  continuous renal
replacement therapy FANS UNJANI YOGYAKARTA
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Standl et al, 2018

16. Invasive haemodynamic measurements
GENERAL SIGNS:
• TACHYCARDIA
• TACHYPNOEA
• CONFUSION
• OLIGURIA
Specific signs : Pulses paradoxus A, Muffled heart
sounds A, Deviated trachea C, New tricuspid
regurgitation B, Raised jugular venous pressure B
A: Cardiac tamponade, B: Massive pulmonary embolism C: Tension
pneumothorax
Causes : Massive pulmonary embolus, Cardiac
tamponade, Tension pneumothorax
Common investigations : Full blood count, urea and
creatinine, electrolytes, clotting studies Arterial
blood gas and lactate, Chest X-ray,
Electrocardiogram
Specific investigations : Echocardiography, CT
pulmonary angiogram
OBSTRUCTIVE SHOCK
INDICATOR VALUE
Cardiac index ⬇
Pulmonary artery occlusion pressure Normal or ⬆
Central venous pressure ⬆
Systemic vascular resistance ⬆
Oxygen delivery ⬇
Song & Soni, 2013; Shagana et al, 2018

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18. OBSTRUCTIVE SHOCK MANAGEMENT
• Obstructive shock needs immediate causal
treatment.
• Simple measures may suffice, such as
changing the position of a patient with caval
compression syndrome or adjusting the
ventilation of the patient where the level of
positive end expiratory pressure (PEEP) is too
high.
• According to the underlying cause of the
obstruction, a pulmonary embolism is treated
with thrombolysis; tension pneumothorax or
pericardial tamponade are relieved
immediately by thoracic or pericardial
drainage (recommendation grade: A); and
Leriche syndrome is treated by surgical
embolectomy.
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Standl et al, 2018; Coy et al, 2015

19. Invasive haemodynamic measurements
GENERAL SIGNS:
• TACHYCARDIA
• TACHYPNOEA
• CONFUSION
• OLIGURIA
Specific signs : Hypotension, Bounding pulse
Warm and flushed, Pyrexial
Causes : Sepsis, Anaphylaxis, Neurogenic,
Addisonian crisis
Common investigations : Full blood count, urea and
creatinine, electrolytes, clotting studies Arterial
blood gas and lactate, Chest X-ray,
Electrocardiogram
Specific investigations : Blood cultures, Urine
cultures, Cerebrospinal fluid culture, Mast cell
tryptase, Magnetic resonance imaging of spine
DISTRIBUTIVE SHOCK
INDICATOR VALUE
Cardiac index ⬆
Pulmonary artery occlusion pressure Normal or ⬇
Central venous pressure Normal or ⬇
Systemic vascular resistance ⬇
Oxygen delivery ⬆
Song & Soni, 2013; Shagana et al, 2018

20. SOFA (Sequential Organ Failure Assessment)
Standl et al, 2018

21. Anaphylactic Shock
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22. Neurogenic Shock Damiani, 2018

23. SEPTIC SHOCK MANAGEMENT
• Support the circulation by the infusion of balanced crystalloid solutions (recommendation grade:
A)
• administration of vasopressors (norepinephrine, vasopressin if needed), in some cases also
inotropic drugs (e.g., dobutamine), and organ replacement therapy (recommendation grade: B)
• Advanced invasive monitoring is indicated to allow tailored therapy for the impaired
hemodynamics  Echocardiography has a central part to play here.
• All sepsis patients, as soon as samples have been obtained for microbiological study, calculated
broad-spectrum antibiotic therapy and (if possible) source control (causal treatment) should be
started as soon as possible (recommendation grade: A).
• Monitoring of non-infectious disease involving extensive mediator activation (e.g., acute
pancreatitis) may lead to a clinical presentation similar to that of septic shock. This is due to
activation of the same mediator cascade by non-infectious molecular signals of soft tissue
damage.
• Know and monitor if there a the toxic shock syndrome (TSS) because it related to a condition of
septic shock. TSS is characterized by fever, severe hypotension, and skin rash as the main
symptoms
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Standl et al, 2018

24. ANAPHYLACTIC SHOCK MANAGEMENT
• Constant monitoring, as late reactions including arrhythmias,
myocardial ischemia, and respiratory failure may manifest as late as
12 hours after the initial event.
• Administration of epinephrine (plus norepinephrine, if necessary) and
forced fluid replacement are required in anaphylactic shock.
• If there a patients with bronchospasm, β-sympathomimetics and, as
second- line treatment, glucocorticoids are indicated (as they are in
patients with delayed progressive symptoms)is required.
• Administer histamine antagonists suppress the histaminergic effects
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Standl et al, 2018

25. NEUROGENIC SHOCK MANAGEMENT
• The critical element in treating neurogenic shock is the treatment of
the cause.
• Rapid fluid replacement (normal saline 0,9%)
• Give norepinephrine with increasing dosages until peripheral
vascular resistance rises  1st line option.
• Restore vascular tone with direct- or indirect-acting
sympathomimetics can also be given.
• Pulse oximeter given high flow oxygen.
• placed in supine or Trendelenburg position to increase blood return
to the heart.
• Give mineralocorticoids to increase plasma volume are also a
therapeutic option.
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Standl et al, 2018; Volski & Ackerman, 2019

26. DRUGS OPTION FOR SHOCK CONDITIONS
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Standl et al, 2018

27. DRUGS OPTION FOR SHOCK CONDITIONS
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Standl et al, 2018

28. DRUGS OPTION FOR SHOCK CONDITIONS
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Standl et al, 2018

29. REFERENCES
• Haberal, M., Sakallioglu Abali, A. E., & Karakayali, H. (2010). Fluid management in major burn injuries. Indian journal of plastic surgery : official
publication of the Association of Plastic Surgeons of India, 43(Suppl), S29–S36. https://doi.org/10.4103/0970-0358.70715
• Eric McCoy, MD, MPH, et al.2015. Leriche Syndrome Presenting with Multisystem Vaso-Occlusive Catastrophe. Volume 16, Issue 4, July
2015. available at https://westjem.com/case-report/leriche-syndrome-presenting-with-multisystem-vaso-occlusive-catastrophe.html
• Standl T, Annecke T, Cascorbi I, Heller AR, Sabashnikov A, Teske W: The nomenclature, definition and distinction of types of shock.
Dtsch Arztebl Int 2018; 115: 757–68. DOI: 10.3238/arztebl.2018.0757
• Shagana et al. 2015. Hypovolemic shock- a review. Available at https://jprsolutions.info/files/final-file-5b3f0331f0f340.99334869.pdf
• John Soong and Neil Soni. 2013. Circulatory Shock. Available at https://www.medicinejournal.co.uk/article/S1357-3039(12)00281-
• DeTurk, S. et al. 2019. Anaphylactic Shock. Available at https://www.intechopen.com/books/clinical-management-of-shock-the-
art-of-physiological-restoration/anaphylactic-shock
• Vahdatpour,C., Collins,D., Goldberg,S. 2019. Cardiogenic Shock. Available at
• Volski,A & Ackerman,D.J. 2019. Neurogenic Shock. Available at https://www.intechopen.com/books/clinical-management-of-shock-
science-and-art-of-physiological-restoration/neurogenic-shock
• Damiani, D. 2018. Neurogenic Shock. Available at https://www.thieme-connect.de/products/ejournals/pdf/10.1055/s-0036-
• Morgan,C and Wheeler,D.S.2013. Available at https://openpediatricmedicinejournal.com/contents/volumes/V7/TOPEDJ-7-35/TOPEDJ-
35.pdf
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30. THANK YOU SO MUCH
Any Questions?
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