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
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
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
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
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
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
Notes: The inadequate perfusion and oxygenation leads to first cellular dysfunction and then organ dysfunction.
-Cellular effects include cell membrane ion pump dysfunction, intracellular edema, leakage of intracellular contents into the
extracellular space, and inadequate regulation of intracellular pH.
-Systemic effects include alterations in the serum pH, endothelial dysfunction, as well as further stimulation of
inflammatory and antiinflammatory cascades that lead to multiorgan dysfunction
Notes:
Mortality due to shock is high. It is estimated that 35 to 60% of patients die within one month of the onset of septic shock. The mortality rate may be even higher among patients with cardiogenic shock; it is estimated to be 60 to 90%. Mortality due to hypovolemic shock is more variable.
Early intervention can prevent the cascade of detrimental effects of O2 deprivation on the cells and organs
Notes:
All forms of shock go through “stages “ of shock. How quickly the patient goes through the stages depends on the cause of shock, patient characteristics, and how quickly we intervene.
For example, a healthy adult can be asymptomatic despite a 10% reduction in total effective blood volume. OR if a healthy patient is bleeding slowly from a bleeding ulcer, he will be able to compensate for the blood loss for a long time. If the blood loss is very rapid (e.g. from splenic rupture in Case 1), the patient may progress to death within minutes going through all stages within minutes to hours
Preshock — Preshock is also referred to as warm shock or compensated shock. It is characterized by rapid
compensation for diminished tissue perfusion by various homeostatic mechanisms. As an example,
compensatory mechanisms during preshock may allow an otherwise healthy adult to be asymptomatic
despite a 10 percent reduction in total effective blood volume. Tachycardia, peripheral vasoconstriction,
and either a modest increase or decrease in systemic blood pressure may be the only clinical signs of shock.
Shock — During shock, the compensatory mechanisms become overwhelmed and signs and symptoms of organ
dysfunction appear. These include tachycardia, dyspnea, restlessness, diaphoresis, metabolic acidosis, oliguria,
and cool clammy skin.
End-organ dysfunction — Progressive end-organ dysfunction leads to irreversible organ damage and patient death.
End organ dysfunction - typically correspond to a significant physiologic perturbation
Examples include a 20 to 25% reduction in effective blood volume in hypovolemic shock, a fall in the cardiac
index to less than 2.5 L/min/M2 in cardiogenic shock, or activation of innumerable mediators of the systemic
inflammatory response syndrome (SIRS) in distributive shock.
During this stage, urine output may decline further (culminating inanuria and acute renal failure), acidemia
decreases the cardiac output and alters cellular metabolic processes, and restlessness evolves into agitation,
obtundation, and coma.
REFERENCES: Up to date - Shock to Adults: Types, presentation, diagnostic approach
Notes: This is a summary slide
Notes: The earlier table was oversimplified. Regardless of the type of SHOCK all components of the equation will compensate for
the physiologic change induced by the insult, however some will be more effective than others
may be considered as the ventricular wall tension required to eject the stroke volume during systole.
Afterload relates to the mechanical resistance to shortening of the cardiac muscle fibers.