explain regarding definition, types and pathophysiology of shock. will be very helpful for med school to do quick read prior to exam

1. SHOCK
PRESENTER: DR ANURA BT AMAN
SUPERVISOR: AP DR MOHD ZULFAKAR BIN MAZLAN

2. Outlines
• Overview of Shock
• Pathophysiology
• Type of shock
• Clinical sign
• Investigation
• Management
• Reference

3. Definition of shock
Acute circulatory failure associated with inadequate oxygen utilization by the cells.
OH’s Intensive Care Manual 8th Edition
Failure to meet the metabolic demands of cells and tissues and the consequences
that ensue.
Failure to deliver and/or utilize adequate amounts of oxygen
Schwartz’s Principles of Surgery

4. Oxygen delivery (DO2)
•Hb is the haemoglobin concentration (g/L)
•SaO2 is the arterial Hb saturation
•PaO2 is the arterial oxygen partial pressure.
Assuming adequate arterial oxygen content, CO becomes the
main determinant of DO2

5. DO2 and VO2 relationship
• Relationship between oxygen delivery and
oxygen consumption (VO2).
• In normal conditions, oxygen delivery meets
the demands of oxygen consumption
(Oxygen supply independency).
• When DO2 drops initially, reserve oxygen
utilized
• Further DO2 decrease, oxygen extraction
from the Hb is increased
• With even further reduction of DO2, oxygen
maximally extracted from Hb, VO2 becomes
dependent on DO2 (oxygen supply
dependence)

6. Dysoxia
Dysoxia occurs beyond the critical point of supply dependency (critical DO2 )
Inadequate oxygen supply leads to
• Anaerobic cellular metabolism
• Less efficient adenosine triphosphate (ATP) production
• Consequent cellular and organ dysfunction.
If dysoxia persists, the ongoing inadequate of oxygen supply affects cell membrane
ion channels, leading to sodium and water influx, cellular oedema, breaching of cell
membrane integrity, cell injury and eventually, cell death.

7. Different organs have their own metabolic requirements
• Heart and brain, higher metabolic demand and high O2 extraction – more vulnerable
• Kidney and skin, lower metabolic demand and low O2 extraction – less susceptible
Dysoxia can still occur despite adequate oxygen delivery,
• Sepsis
• Multiorgan dysfunction syndrome
Arteriolar shunting around the microvascular capillary beds prevents oxygen
delivery to the cells, and inflammatory mediators induce mitochondrial dysfunction,
which preventing cells from utilizing the available oxygen.
Therefore, hypotension not required to define shock

8. PATHOPHYSIOLOGY OF SHOCK
• Shock is a clinical state of acute circulatory failure
• Results from 4 mechanisms (also in combinations)
• Loss of circulating volume
• Pump dysfunction
• Obstruction
• Maldistribution of blood due to a lack of vascular tone

9. • Imbalances in cellular supply and demand leads to changes in
• Cardiovascular system
• Microcirculation
• Neuroendocrine response
• Immune and inflammatory responses
• Metabolic
• Acid base balance
Pathophysiology of shock

10. Cardiovascular response
Loss of intravascular volume causes reduced MAP
↓
Baroreceptors in the aortic arch and carotid bodies detect
↓
Sympathetic activation in vasomotor centres
↓
Cathecholamines released from adrenal medulla
↓
Increased HR and myocardial contractility, vasoconstriction
↓
Increased TPR and blood pressure
Pathophysiology of shock

11. Microcirculation
Pathophysiology of shock

12. Neuroendocrine response
• Main goal is to maintain perfusion to heart
and brain
• Multiple stimuli (pain, hypercarbia,
hypoxia, hypotension, hypoglycemia,
acidosis) can trigger a response
• Hypothalamic-pituitary-adrenal axis and
autonomic system activated
• ACTH leads to cortisol release
(gluconeogenesis, insulin resistance and
lipolysis)
• Angiotensin II stimulates vasoconstriction
• Aldosterone for sodium reabsorption
• ADH(vasopressin) for water reabsorption
Pathophysiology of shock

13. Immune and inflammatory responses
• Can be cause or sequalae of shock due to hypoperfusion
• Caused by direct tissue injury or infection
• Release of intracellular products from damaged or injured cells trigger
inflammatory response and cytokine release
• TNF alpha – peripheral vasodilation, procoagulant activity
• IL-1 – febrile response, stimulate release of other cytokines
• IL-6 – diffuse alveolar damage and ARDS
• Complement cascade activation – increased vascular permeability, adherence
of neutrophils vascular endothelium, ARDS and MODS
Pathophysiology of shock

14. Metabolic
• ATP is generated via oxidative phosphorylation in mitochondria
• Insufficient oxygen leads to anaerobic metabolism (cellular
glycogen broken down to pyruvate) – poorer yield of ATP
• Pyruvate converted to lactate – lactic acidosis
• Lower pH influences vital cellular functions such as normal
enzyme activity, cell membrane ion exchange, and cellular
metabolic signaling
• Irreversible cell injury and cell death
Pathophysiology of shock

15. Acid base balance
• Low pH and high lactate levels indicate tissue hypoperfusion
• Respiratory and renal mechanisms compensate the metabolic acidosis to a certain degree
• In shock, renal perfusion is impaired, causing renal failure and worsening acidosis
Pathophysiology of shock

16. Pathophysiology of shock
• Initial pathophysiological response to maintain hemostasis – compensated shock
• Continued hypoperfusion cause ongoing cell injury and death – decompensated shock
• Microcirculatory dysfunction, parenchymal tissue damage, and inflammatory cell
activation can perpetuate hypoperfusion, leading to vicious cycle (irreversible shock)

17. TYPES OF SHOCK

18. • Impairment of circulatory supply of oxygen to the cells is commonly classified
according to which component of the circulation is primarily disturbed, that is:
Hypovolemic shock
(inadequate preload)
Cardiogenic shock
(pump failure)
Vasodilatory/distributive shock
(altered vascular capacitance)

19. 1. Hypovolemic shock
Acute blood loss or
excessive fluid losses
Decreased circulating
blood volume
Reduced preload &
SV (stroke volume)
Invokes
cardiovascular
compensatory
mechanism

20. ↑ venous tone
The venous system holds ≈80% of blood volume
& acts as a blood reservoir. The SNS controls
venous tone & capacitance of the venous system.
↓capacitance favours venous return to the heart in
an attempt to maintain SV
↑ arteriolar tone
Sympathetic stimulation of arteriolar resistance
vessels ↑ perfusion pressure to the organs.
↑ HR
To compensate SV ↓, HR ↑ in order to maintain
SV
↑ contractility
Heart will contract vigorously to ↑SV
& maintain CO
CARDIOVASCULAR
COMPENSATORY
MECHANISM

21. Causes of hypovolemic shock
Blood Loss Fluid Loss
❑ Vascular injury (e.g trauma, surgery)
❑ GI bleeding (e.g peptic ulcer, diverticular, angio-
dysplasia varices)
❑ Obstetric bleeding (e.g placenta previa, postpartum
hemorrhage)
❑ Intra-abd hemorrhage (e.g splenic laceration, liver
injury)
❑ Retroperitoneal (e.g aortic aneurysm, ectopic
rupture, femoral artery bleeding, pelvic #)
❑ Long bone #
❑ Pulmonary hemorrhage, heamothorax
❑ Vomiting
❑ Diarrhea
❑ Ileostomy losses
❑ Sweating
❑ Polyuria (e.g glucosuria, diabetes
insipidus)
❑ Burns
❑ Pancreatitis

22. Pathophysiology
• Increasing venous tone
(venoconstriction)
• Increasing arteriolar tone
– by sympathetic
stimulation.
• Increasing HR (CO= SV x
HR), to compensate the
reduction of SV
• Increasing contractility

23. 2. Cardiogenic shock
The heart is the main supply of circulatory supply of oxygen and if the pump fails,
then little compensatory mechanisms remain.
Hence, cardiogenic shock has high mortality (45% - 100%)
Treatment: urgent correction of underlying acute cardiac disease & consideration of
afterload reduction while ensuring adequate organ perfusion

24. Causes of cardiogenic shock
❑ Myocardial ischaemia
❑ Acute valve dysfunction (e.g chordae rupture, prosthetic valve thrombus)
❑ Myocarditis
❑ Contusion
❑ Septal/ventricular rupture
❑ Drugs (e.g Ca2+ channel blocker overdose, B-blocker overdose)
❑ Extrinsic compression (e.g tension pneumothorax, tamponade)
❑ Pulmonary emboli, pulmonary hypertension
❑ Bradyarrythmias (e.g complete heart block)
❑ Tchyarrythmias (e.g atrial or ventricular tachycardias)

25. 3. Obstructive shock
Mechanical obstruction to the flow of blood through the cardiac chamber will lead
to reduced cardiac output.
Treatment is urgent removal of obstruction (e.g drainage of pericardial effusion,
lysis of thromboembolism)
Causes of obstructive shock
❑ Obstruction (e.g valve thrombosis, myxoma)
❑ Extrinsic compression (e.g tension pneumothorax, cardiac tamponade)
❑ Cardiac outflow obstruction (e.g pulmonary embolus, hypertrophic obstructive
cardiomyopathy

26. 3. Distributive shock
Arteriolar autoregulation, the autonomic NS & vasoactive hormones control the distribution
of blood around the vascular network
Distributive shock result from failure of these mechanism, leading to inappropriate blood
distribution
Unline any other tyoe of shock, distributive shock may have increase cardiac output initially
to compensate of maldistributive of blood
Treatment are to identify & treat the precipitating cause and to improve the organ perfusion
with fluid resus & vasoactive drugs

29. CLINICAL SIGNS
Clinical features of shock reflect the inadequate circulation & insufficient oxygen
distribution:
⮚HYPOTENSION
⮚TACHYCARDIA
⮚TACHYPNOEA
⮚OLIGURIA
⮚ALTERED MENTAL STATUS
⮚IMPAIRED PERIPHERAL PERFUSION

30. INVESTIGATIONS
Bedside
• Haemoglobin
• Arterial blood gas
• Lactate
• ECG
• USG (e.g. Fast scan,
AAA scan)
• Echocardiogram
Laboratory
• FBC, Coag profile, D-
dimer
• Electrolytes, RFT,
LFT
• Cardiac enzymes,
lipase
• Cultures (urine,
blood, sputum, pus)
• Toxicology assays
Radiology
• CXR, AXR
• Trauma series
radiology (chest,
pelvic, cervical spine)
• CT
• Angiography (e.g
coronary, visceral,
pulmonary)

31. MANAGEMENT
Resuscitation of shock is a medical emergency
Aim: to restore the systemic DO2 effectively & rapidly
❑ Ensure Adequate Oxygenation
❑ Vascular Access
❑ Fluid Resuscitation
❑ Cardiovascular Medication
❑ Manage Precipitating Illness/injury
❑ Monitoring (frequent assessment of HR, BP, RR, conscious state, Urine output, T,
peripheral perfusion)

32. a. Ensure Adequate Oxygenation
Ensure adequate FiO2 and SaO2
and correct any reversible cause of
pulmonary shunt (e.g. pleural
collection, bronchus obstruction)
b. Vascular Access
Cannula size plays an important
intravenous access as it plays major
implications for the rate of laminar
fluid flow.

33. This emphasis the effect of radius & cannula
length on flow. Hence, its advisable to use short,
wide-bore catheters for rapid IV administration.
A central venous cannula should be considered
in patients with persistent shock, particularly if
they requiring the infusion of drugs (e.g
catecholamine, cardiovasc medication, multiple
infusion) beside patient with difficult peripheral
venous cannula

35. c. Fluid Resuscitation
i. Trendelenburg Manouvre
ii. Crystalloid Solutions
iii. Albumin Solutions
iv. Starch Solution
v. Red Blood Cell

36. i. Trendelenburg Manouvre
A quick method to increase venous return
is to till the patient's pelvis above
horizontal (i.e. head down)
This will 'auto-transfuse' blood from leg
and pelvic veins into central veins,
augmenting preload.
The hemodynamic response to this
manouvre can be used whether fluid
resus will enhance cardiac output.

37. c. Fluid Resuscitation
Fluid resuscitation should be administered in titrable aliquots
& haemodynamically response should be assess from time to
time ( to prevent hypervolemia & its consequences)
Its important to remember that not all patient will responds to fluid loading
with significant increase CO. If the heart is working on the terminal
(flat)portion of the Frank-Starling curve, increased preload will not result
in a significant increase in SV.
Further-more, the relationship between preload and stroke volume is
dynamic and is affected by many other variables extrinsic to the heart (e.g.
autonomic tone,cardiovascular medications, ventilation, lung
disease)These need to be considered when determining thevolume of fluids
to administer.

38. Types of IV Fluid:
• Crystalloids vs Colloids
• Type of crystalloids
• Isotonic / hypotonic / hypertonic
• Type of colloids
• Fluids vs blood
Recommends to restore euvolemia with IV fluids more urgently initially
then more cautiously as the patient stabilizes.

39. ii. Crystalloid Solutions
Made up of electrolytes (with or without dextrose) and water
Easily cross semipermeable membranes & rapidly distributed through
intravascular and extravascular spaces
Factors effecting fluid equilibration across the body compartments:
• Osmolality of the fluid
• Solute clearance
• Integrity of the vascular endothelium

41. Crystalloid Uses Disadvantages
NaCl 0.9%
Commonly used for initial volume
replacement
Slightly hyperosmolar (300 mOsm/L) and
hyperchloraemic (150 mEq/L) relative to
plasma.
Hyperchloraemia can contribute to bicarbonate loss
and a normal anion gap metabolic acidosis.
Lactated Ringer’s Solution
(Hartmanns)
Isotonic and contains lactate
(29 mEq/L) and electrolytes in a ratio
similar to plasma.
The calcium in Hartmann’s (4 mEq/L) is incompatible
with certain drugs
Lactate levels may rise if hepatic function is
markedly impaired or a lot of fluid is administered.
Concentrated Saline
NaCl 7.5%
a small volume can increase circulating
volume
(e.g. 250 mL 7.5% saline can increase
circulating volume by 500 mL)
The sodium also passes into interstitial space leading
to increased interstitial fluid volume, at the expense
of intracellular volume.
Volume resuscitation with hypertonic saline may
prevent cerebral oedema, but a recent clinical trial of
its use in head-injured patients did not show
improved outcomes.

42. Colloids
Colloids are solutions containing large molecules that do not pass through a
semipermeable membrane
Remains in the circulation for longer, have a smaller volume of distribution
Hence, more effective at increasing intravascular volume than the same volume
of crystalloid.
2 major groups of colloids
Plasma derivatives
• Human albumin
• Plasma protein fraction
• Fresh frozen plasma
• Immunoglobulin solutions
Semi-synthetics
• Gelatins
• Dextrans
• Hydroxyethyl starches (HES).

43. iii. Albumin Solutions
4% normal serum albumin (NSA 40g/L; 260 mOsm/L)
is iso-oncotic and infusion increases circulating
volume.
NSA is a byproduct of whole blood separation.
Concentrated (20%) albumin is available in smaller
volume (100mL) – it increases the fluid volume by
drawing fluid from the interstitium, but this process
takes time & not suitable for resuscitation
Risk of transmission of infectious agents

44. iv. Starch Solution
Starch solution contain carbohydrate polymer (starch)
as their oncotic molecule & differ according to their
molecular size of starch used
• 450,000D (high)
• 200,000D (medium)
• 70,000D (low)
Provide effective intravascular volume replacement.
However, it potentially has increased of death, renal
impairment, risk of bleeding – used in septic shock
patient.

45. d. Cardiovascular medication
• When fluid resus fail to restore
adequate DO2, we should
consider to augment the
circulation with catechoamine
agent (inotrope). In severe
shock, it may be need to
commence fluid resus &
vasoactive therapy
concurrently

46. v. Red Blood Cell
• Blood transfusion is essential in
correcting any acute blood loss or
anemia that may contribute to
impaired DO2

47. Manage precipitating illness/injury
Beside the circulation is being restored, the cause of circulatory disturbance need to
corrected
Time to definitive treatment of cause of shock is related to survival. E.g cardiogenic
shock (time reperfusion), hemorrhagic shock (time to hemostasis) & septic shock
(time to appropriate antibiotic)

48. Monitoring
Clinical monitoring involves frequent assessment of:
o HR
o BP
o RR
o GCS
o Urine output
o Peripheral perfusion
o Temperature

49. Arterial cannula
Useful measuring BP, permitting sampling for ABG
(pH, lactate measurement)
Central venous cannula (CVC) allows central venous
pressure (CVP) monitoring (used to estimate preload).
However, CVP bears variable relationship to venous
volume, as it depends on:
o Location of catheter to the right atrium
o Intrathoracic pressure
o Venous compliance
o Position of patient
o Tricuspid valve competence
Thus, CVP does not predict whether administering
a volume fluid will change CO or DO2.

50. Sepsis

51. DEFINITIONS
1. Sepsis:
• A life-threatening organ dysfunction caused by a dysregulated host
response to infection
2. Organ dysfunction:
• Acute change in total SOFA ≥ 2 points due to infection
3. Septic Shock:
• subset of sepsis with circulatory and cellular/metabolic abnormalities are
associated with increased mortality (>40%)
• Sepsis with persisting hypotension (requiring vasopressors to maintain
MAP >65mmHg) and hyperlactatemia (>2mmol/L) despite adequate
volume resuscitation.

52. Sepsis-related Organ Failure Assessment (SOFA)
Score

53. Quick SOFA
If you need to
be quick, use
the QUICK
SOFA

54. Pathophysiology
• Host-microbe equilibrium disrupted leading to infection
• Inflammatory mediators and cells cause dysfunction of endothelium and vasculature
• Leads to vasodilatation and hypotension
• Upregulation in nitric oxide synthase causing increased nitric oxide production for longer periods
(potent vasodilator)
• Most commonly caused by Gram +ve bacteria;
Can also caused Gram negative bacteria.
• Common Gram positive bacteria
• Staph aureus
• Strep pyogenes
• Gram negative
• E coli
• P aureginosa

55. How bacteria
causing sepsis?
• Multiple virulence factors, most
importantly is toxin
• Type of toxin
• Exotoxins
• Mainly by gram
positive bacteria
• Endotoxin – lipo-poly-
saccharides
• Present in the outer
membrane of gram
negative bacteria

66. Reference
KEY REFERENCES
• 1. Cecconi M, De Backer D, Antonelli M, et al.Consensus on circulatory shock and hemodynamicmonitoring, Task force of the European Society of
Intensive Care Medicine. Intensive Care Med.2014;40(12):1795-1815.
• 3. Vincent JL, De Backer D. Circulatory shock. N EnglJ Med. 2013;369(18):1726-1734.
• 6. Myburgh JA, Mythen MG. Resuscitation fluids.N Engl J Med. 2013;369(13):1243-1251.
• 15. Perner A, Haase N, Guttormsen AB, et al.Hydroxyethyl starch 130/0.42 versus Ringer'sacetate in severe sepsis. N Engl J Med. 2012;367(2):124-134.
• 16. MyburghJA, Finfer S, Bellomo R, et al. Hydroxyethylstarch or saline for fluid resuscitation in intensivecare. N Engl J Med. 2012;367(20):1901-1911.
• 30. Marik PE, Cavallazzi R. Does the central venouspressure predict fluid responsiveness? An updated.meta-analysis and a plea for some common
sense.Crit Care Med. 2013;41(7):1774-1781.
• 33. Vallet B, Pinsky MR, Cecconi M. Resuscitation ofpatients with septic shock: please 'mind the gap'!Intensive Care Med. 2013;39(9):1653-1655.
• 35. McLean AS. Echocardiography in shockmanagement. Crit Care. 2016;20:275.
• 36. McGee WT, Raghunathan K, Adler AC. Utility offunctional hemodynamics and echocardiographyto aid diagnosis and management of shock.
Shock.2015;44(6):535-541.

67. Thank You For
Your Attention
Have A Good Day