Shock precedes Death and organ failure.

1. Shock
Dr SAM GEORGE
CONSULTANT ANAESTHESIA & INTENSIVE CARE

2. Overview
Definitions
Initial Assessment – ABC
Stages of Shock
Physiologic Determinants of Shock
Types of Shock
Common Features of Shock
Work-up
Generic Approach to Management
Case scenarios and Management
Take Home Points

3. Definition of Shock
Inadequate perfusion and oxygenation of cells
Hypotension is not a requirement

4. Why should you care?
High mortality - 20-90%
Early on the effects of O2 deprivation on the cell are
REVERSIBLE
Early intervention reduces mortality

5. Remember!
Assessment Intervention and Monitoring happens
together in acute scenarios.

6. Initial Assesment - ABC
Airway:
 Does pt have mental status to protect airway?
 GCS less than “eight” means “intubate”
 Airway is compromised in anaphylaxis
Breathing:
 If pt is conversing with you, A & B are fine
 Place patient on oxygen
Circulation:
 Vitals (HR, BP)
 2 large bore (#16g) IV, start fluids (careful if cardiogenic shock), put
on continuous monitor

7. ABC “DE”
In a trauma, perform ABCDE, not just ABC
Deficit or Disability
 Assess for obvious neurologic deficit
 Moving all four extremities? Pupils?
 Glascow Coma Scale (M6, V5, E4)
Exposure
 Remove all clothing on trauma patients

8. TYPES OF SHOCK
Type of Shock Insult Physiologic
Effect
Compensation
Cardiogenic Heart fails to pump blood out
•MI, arrhythmia, aortic stenosis,
mitral regurg,
↓CO BaroRc
↑SVR
Obstructive Heart pumps well, but the
outflow is obstructed
•Extracardiac obstructive causes
such as PE, tension
pneumothorax, tamponade
↓CO BaroRc
↑SVR
Hypovolemic Heart pumps well, but not
enough blood volume to pump
•Hemorrhage
•Fluid Loss (Vomiting, Diarrhea,
Burns)
↓CO BaroRc
↑SVR
Distributive Heart pumps well, but there is
peripheral vasodilation
•Septic, anaphylactic, and
neurogenic shock
•Pancreatitis, burns, multi-trauma
via activation of the
inflammatory response
↓SVR ↑CO

9. Stages of Shock
Timeline and progression will
depend on:
-Cause
-Patient Characteristics
-Intervention
Insult
Preshock
(Compensation)
Shock
(Compensation
Overwhelmed)
End organ
Damage
Death

10. Stages of Shock: Example
Stage Pathophysiology Clinical Findings
Insult Splenic Rupture -- Blood Loss Abdominal tenderness and girth
Preshock Hemostatic compensation
MAP =↓CO(HR x↓SV) x ↑ SVR
Decreased CO is compensated
by increase in HR and SVR
MAP is maintained
HR will be increased
Extremities will be cool due to
vasoconstriction
Shock Compensatory mechanisms
fail
MAP is reduced
Tachycardia, dyspnea,
restlessness
End
organ
dysfuncti
on
Cell death and organ failure Decreased renal function
Liver failure
Disseminated Intravascular
Coagulopathy
Death

11. Common Features of Shock
Hypotension (not an absolute requirement)
 SBP < 90mm Hg, not seen in “preshock”
Cool, clammy skin
 Vasoconstrictive mechanisms to redirect blood from periphery to
vital organs
 Exception is warm skin in early distrib. shock
Oliguria (↓kidney perfusion)
Altered mental status (↓brain perfusion)
Metabolic acidosis

12. Hypovolemic
Shock
Distributive
Shock
Cardiogenic
Shock
Obstructive
Shock
HR Increased Increased
(Normal in
Neurogenic
shock)
May be increased
or decreased
Increased
JVP Low Low High High
BP Low Low Low Low
SKIN Cold Warm (Cold in
severe shock)
Cold Cold
CAP
REFILL
Slow Slow Slow Slow

13. Type of
Shock
Insult Physio
logic
Effect
Compen
sation
Compensation
Heart Rate
Compensation
Contractility
Cardiogenic Heart fails to
pump blood
out
↓CO BaroRc
↑SVR
↑ ↑
Obstructive Heart pumps
well, but the
outflow is
obstructed
↓CO BaroRc
↑SVR
↑ ↑
Hemorrhagic Heart pumps
well, but not
enough blood
volume to
pump
↓CO BaroRc
↑SVR
↑ ↑
Distributive Heart pumps
well, but
there is
peripheral
vasodilation
↓SVR ↑CO ↑
No Change -
in neurogenic
shock
↑
No Change -
in neurogenic
shock
Compensatory Mechanisms

14. Additional Compensatory
Mechanisms
Renin-Angiotensin-Aldosterone Mechanism
 AII components lead to vasoconstriction
 Aldosterone leads to water conservation
ADH leads to water retention and thirst
Inflammatory cascade

15. Work-up
History to determine etiology
 Bleeding (recent surgery, trauma, GI bleed)
 Allergies or prior anaphylaxis
 Sx consistent with pancreatitis, EtOH history
 Hx of CAD, MI, current chest pain/diaphoresis
Examination
 Mucous membranes, JVD, lung sounds, cardiac exam, abdomen,
rectal (blood), neuro exam, skin (cold & clammy or warm)
Investigations: Labs/Tests directed toward suspected dx’s

16. GENERIC APPROACH TO
MANAGEMENT OF SHOCK
OPTIMISE OXYGEN CONTENT
OPTIMISE CARDIAC OUTPUT
OPTIMISE BLOOD PRESSURE
OPTIMISE REGIONAL BLOOD FLOW

17. In Short
 The oxygenated blood carried forward by the
cardiac output has to reach the Vital organs,
 this is only possible if there is a good pressure
gradient
 and the organ vascular resistance is low;
 try to maintain the Blood pressure within the
regional Auto regulation range,
 I prefer to target the kidneys as they are a filter and
require higher mean arterial pressures, essentially
ensures all other organs are also perfused

18. OPTIMISE OXYGEN CONTENT
Hb
Check if appears pale or anaemic
Check Hb and coagulation status
Sao2
just a pulse oximeter tells you the SpO2
Check SaO2 on ABG

19. OPTIMISE CARDIAC OUTPUT
CO = Stroke volume (SV) x Heart rate (HR)
STROKE VOLUME depends on
Preload
Contractility
Afterload

20. Check each component of
Cardiac Output
 Stroke Volume (depends on 3 factors)
 Preload
 Look at response to fluid bolus
 If improves BP could be suggestive of
decreased preload (volume) and a
reasonable contractility.
 If no improvement or worsening BP could be
suggestive of a Contractility problem or excess
preload (volume) situation
 Look at CVP

21. Check each component of
Cardiac Output
 Contractility
 Check any history suggestive of Ischaemic
disease or CCF
 Check ECHO and ECG results
 A high systolic pressure could be suggestive of
good contractility

22. Check each component of
Cardiac Output
 Afterload
 Check Echo if suggestive of any obstructive
features
 If peripheries cold could indicate increased
vascular resistance
 If peripheries warm could indicate vasodilation
and decreased vascular resistance
 a low diastolic Blood pressure could indicate low
vascular resistance
 a high diastolic Blood pressure could indicate
increased vascular resistance

23. Check each component of
Cardiac Output
 HR
 If low, 2 possible interventions
 electric
 pacing
 pharmacological intervention
 if high, 2 possible interventions
 electric
 cardioversion
 Defibrillation
 pharmacological intervention

24. OPTIMISE BLOOD PRESSURE
Product of Cardiac output and peripheral
resitance.
BP=CO X PR

25. OPTIMISE REGIONAL BLOOD
FLOW
Improve Blood pressure, which is a product of
 Cardiac Output
 peripheral resistance (squeeze)
Improve, Regional Blood Flow = (p1-p2) / R, i.e.
by increasing Mean Arterial pressure decreasing
venous or the compartment pressure whichever
is higher, and also decreasing the organ vascular
resistance

26. Auto regulation range
try to match Renal auto regulation range
 Kidneys
 MAP 80-180 mmHg
 Brain
 MAP 65-130 mmHg
 Heart
 MAP 50-150 mmHg
 If hypertensive Autoregulation values could shift to
right, essentially you will need Higher MAP (mean
arterial pressure) to perfuse the vital organs.

27. Case 1
55yo male otherwise healthy who is fresh post-op
from a colon resection for CA
Called for tachycardia, hypotension, altered
mental status, and abd distension
On exam: pale, dry mucous membranes,
disoriented, abdomen is tender and tense
UOP is 15mL over past hour
What else do you want to know?
What is the most likely diagnosis?

28. Case 1
The one thing you want to know: Hct (Hgb)
Dx: Hemorrhagic (hypovolemic) shock
Management
 ABC (need intubation? IV access?)
 Wide open fluids and T&C 6 units PRBC
 Send coags when sending for CBC
 Make sure it’s not an MI (chest pain, EKG)
 Give blood & prepare for re-exploration in OR

29. Case 2
75yo male PMH CAD, PVD, DM who is post-op
from AAA repair complains of crushing substernal
chest pain
Stat 12-lead EKG shows ST elevation in 2
contiguous leads
What do you do?
What is the diagnosis?

30. Case 2
ABC, get good access, continuous monitor
Dx: Acute ST elevation MI
Treatment: “MONA”
 Oxygen, Aspirin, Nitroglycerin, Morphine
 Beta-blockade (no heparin or tPA due to surg)
 Plavix & GP IIb/IIIa inhibitor (i.e. eptifibatide)
 Stat cardiology consult for cardiac cath

31. Case 2, continued
Cath reveals critical stenosis of left main s/p
balloon angioplasty
24 hrs later, in ICU intubated
Vitals: 80/50
On exam: cool, clammy extremities
Echocardiogram: severe LV dysfunction
What is the diagnosis & management?

32. Case 2, continued
Dx: Cardiogenic shock 2ndary to STEMI
Management
 RESUSCITATIVE CARE (remember, ABC)
 SUPPORTIVE CARE Ventilator support Inotropes and
Vasopressors Cardiac output monitoring to optimize
volume status and cardiac function
 May need intra-aortic balloon pump
 DEFINITIVE CARE
 PCI Thrombolysis, Aspirin, Heparin (maintain coronary
patency)

33. Case 3
60yo male heavy drinker brought in by EMS with nausea,
vomiting, severe epigastric pain radiating to the back
Tachycardic, hypotensive
Altered mentation, dry mucous membranes, minimal UOP after
Foley
What is the most likely diagnosis?
 Differential diagnosis?
How do you manage this patient?

34. Case 3
Acute pancreatitis
 DDx of acute abdomen: Perforated viscus, acute mesenteric
ischemia, cholecystitis, SBO, Ruptured AAA, MI
Hypovolemic shock from vomiting and Distributive shock from
the inflammation: vasodilation, vasopermeability (3rd
-space)
Management
 RESUSCITATIVE CARE (remember, ABC) These pts require heavy,
heavy fluid resus
SUPPORTIVE CARE NPO, NGT feed post-pyloric, consider CT
scan
DEFINITIVE CARE

35. Case 4
55yo male also post-op from colon resection for
CA, epidural placed for post-operative pain
control
Called by nurse for hypotension and
bradycardia
Abdomen soft, no pallor, altered mentation
Hct is 38
Most likely diagnosis?

36. Case 4
Neurogenic shock 2ndary to epidural
Differentiated from hypovolemic due to bradycardia
Management
 RESUSCITATIVE CARE (remember, ABC) IVF
 SUPPORTIVE CARE If BP does not respond, then alpha-agonist such as
phenylephrine until above measures stabilize patient, then wean the
vasopressor
 DEFINITIVE CARE Turn down or turn off epidural,

37. Case 5
25yo male presents with diffuse abdominal pain
of 1day duration, started initially as epigastric
pain after a meal. Takes ibuprofen 3x a day.
Vitals: hypotensive, tachycardic
Tense abdomen, involuntary guarding, altered
mental status, oliguric
What is the diagnosis & management?

38. Case 5
Septic shock 2ndary to perf duodenal ulcer
 This patient has diffuse peritonitis
Management:
Management
 RESUSCITATIVE CARE (remember, ABC) IV & resuscitation (requires
heavy fluids)
 SUPPORTIVE CARE If pt, does not respond to fluids, may need
vasopressors (norepinephrine)
 Have beta-agonist effects to help pump function as well as alpha-
agonist for periph vasoconstriction
 DEFINITIVE CARE
 Broad-spectrum IV antibiotics
 Emergent OR for ex-lap, washout & repair

39. Take Home Points
Shock = poor tissue perfusion/oxygenation
Know difference btw compensated/uncomp shock
3 types are based on physiology of shock
Hypovolemic due to decreased preload
Cardiogenic due to decreased SV or CO
Distributive due to decreased SVR
Know the common signs a/w shock
Oliguria, AMS, cool/clammy skin, acidosis
Work-up & management starts with ABC
Aggressive resuscitation except if cardiogenic
Vasopressors if hypotensive despite fluids

40. Thanks

41. MAP
Diastolic + 1/3 Pulse pressure

42. REGIONAL BLOOD FLOW
FLOW= P1-P2 / R
P1= MAP
P2= VENOUS PRESSURE

43. REGIONAL BLOOD FLOW
CORONARY BLOOD FLOW=
AORTIC ROOT DIASTOLIC PRESSURE-LVEDP
---------------------------------------------------CORONARY
VASCULAR RESISTANCE
CEREBRAL BLOOD FLOW=MAP-CVP/ICP
-----------------
C.VASC.RESISTANCE