3. Definition of ShockDefinition of Shock
• Inadequate perfusion and oxygenation of cells leads to:
o Cellular dysfunction and damage
o Organ dysfunction and damage
4. Why should you care?Why should you care?
• High mortality - 20-90%
• Early on the effects of O2 deprivation on the cell are
REVERSIBLE
• Early intervention reduces mortality
12. Obstructive Shock:Obstructive Shock:
CausesCauses
↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR
• Heart is working but there is a block to the outflow
o Massive pulmonary embolism
o Aortic dissection
o Cardiac tamponade
o Tension pneumothorax
• Obstruction of venous return to heart
o Vena cava syndrome - eg. neoplasms, granulomatous disease
o Sickle cell splenic sequestration
18. Distributive Shock:Distributive Shock:
CausesCauses
↓MAP = ↑CO (HR x SV) x ↓ SVR
• Loss of Vessel tone
o Inflammatory cascade
• Sepsis and Toxic Shock Syndrome
• Anaphylaxis
• Post resuscitation syndrome following cardiac arrest
o Decreased sympathetic nervous system function
• Neurogenic - C spine or upper thoracic cord injuries
o Toxins
• Due to cellular poisons -Carbon monoxide, methemoglobinemia,
cyanide
• Drug overdose (a1 antagonists)
19. To SummarizeTo Summarize
Type of
Shock
Insult Physiologic
Effect
Compensation
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
20. Ok…itOk…it’s really not THAT’s really not THAT
simplesimple
MAP = CO x SVR
HR x Stroke volume
Preload Afterload Contractility
21. 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
23. Stages of ShockStages of Shock
Timeline and progression will
depend on:
-Cause
-Patient Characteristics
-Intervention
Insult
Preshock
(Compensation)
Shock
(Compensation
Overwhelmed)
End organ
Damage
Death
24. Is this Shock?Is this Shock?
• Signs and symptoms
• Laboratory findings
• Hemodynamic measures
25. Symptoms and Signs ofSymptoms and Signs of
ShockShock
• Level of consciousness
• Initially may show few symptoms
o Continuum starts with
• Anxiety
• Agitation
• Confusion and Delirium
• Obtundation and Coma
• In infants
o Poor tone
o Unfocused gaze
o Weak cry
o Lethargy/Coma
o (Sunken or bulging fontanelle)
26. Symptoms and Signs ofSymptoms and Signs of
ShockShock
• Pulse
o Tachycardia HR > 100 - What are a few exceptions?
o Rapid, weak, thready distal pulses
• Respirations
o Tachypnea
o Shallow, irregular, labored
27. • Blood Pressure
o May be normal!
o Definition of hypotension
• Systolic < 90 mmHg
• MAP < 65 mmHg
• 40 mmHg drop systolic BP from from baseline
• Children
o Systolic BP < 1 month = < 60 mmHg
o Systolic BP 1 month - 10 years = < 70 mmHg + (2 x age in years)
• In children hypotension develops late, late, late
o A pre-terminal event
Symptoms and Signs of Shock
28. Symptoms and Signs ofSymptoms and Signs of
ShockShock
• Skin
o Cold, clammy (Cardiogenic, Obstructive, Hemorrhagic)
o Warm (Distributive shock)
o Mottled appearance in children
o Look for petechia
• Dry Mucous membranes
• Low urine output <0.5 ml/kg/hr
30. Empiric Criteria for ShockEmpiric Criteria for Shock
4 out of 6 criteria have to be met
• Ill appearance or altered mental status
• Heart rate >100
• Respiratory rate > 22 (or PaCO2 < 32 mmHg)
• Urine output < 0.5 ml/kg/hr
• Arterial hypotension > 20 minutes duration
• Lactate > 4
31. LactateLactate
• Lactate is increased in Shock
• Predictor of Mortality
• Can be used as a guide to resuscitation
o However it is not necessary, or available in many settings
32. Management of ShockManagement of Shock
• History
• Physical exam
• Labs
• Other investigations
• Treat the Shock - Start treatment as soon as you
suspect Pre-shock or Shock
• Monitor
33. Historical FeaturesHistorical Features
• Trauma?
• Pregnant?
• Acute abdominal pain?
• Vomiting or Diarrhea?
• Hematochezia or hematemesis?
• Fever? Focus of infection?
• Chest pain?
40. Stages of ShockStages of Shock
Early Intervention can arrest or
reduce the damage
Insult
Preshock
(Compensation)
Shock
(Compensation
Overwhelmed)
End organ
Damage
Death
41. TreatmentTreatment
• ABC’s “5 to 15”
o Airway
o Breathing
o Circulation
o Put the patient on a monitor if available
• Treat underlying cause
43. • Consider Intubation
o Is the cause quickly reversible?
• Generally no need for intubation
o 3 reasons to intubate in the setting of shock
• Inability to oxygenate
• Inability to maintain airway
• Work of breathing
Treatment: Airway and Breathing
47. Blood ProductsBlood Products
• Use blood products if no improvement to fluids
o PRBC 5-10 ml/kg
• O- in child-bearing years and O+ in everyone else
o +/- Platelets
49. Can we measure cellCan we measure cell
hypoxia?hypoxia?
• Lactate - we already talked about - a surrogate
• Venous Oxygen Saturation - more direct measure
51. Venous OxygenVenous Oxygen
SaturationSaturation
• Svo2 = Mixed venous oxygen saturation
o Measured from pulmonary artery by Swan-Ganz catheter.
Normal > 65%
• Scvo2 = Central venous oxygen saturation
o Measured through central venous cannulation of SVC or R
Atrium - i.e. Central Line
Normal > 70%
52. Concluding RemarksConcluding Remarks
• Know how to distinguish different types of shock and
treat accordingly
• Look for early signs of shock
• SHOCK = hypotension
53. Concluding RemarksConcluding Remarks
• Choose cost effective and high impact interventions
• Do not need central lines and ScvO2 measurements
to make an impact!!
54. Concluding RemarksConcluding Remarks
• ABC’s “5 to 15”
o Can’t intubate?
• Give oxygen
• Develop algorithms for bag valve mask ventilation
• Treat fever to decrease respiratory rate
o Treat early with fluids - need lots of it!!
55. Concluding RemarksConcluding Remarks
• Monitor the patient
o Do not need central venous pressure and ScvO2
o Use the HR, MAP, mental status, urine output
o Lactate clearance?
Instructions:
1. We recommend taking the learners through this module in two sittings - Part 1 and Part 2
2. Depending on the level of training of the learner, you may use slides 5-25 as a review or skip them completely and proceed to Case 1 in slide 26.
3. In the notes sections we provide supplementary information and evidence that can be used to supplement the teaching session depending on the level of the learners
Notes: Another way to describe Shock is as an imbalance between O2 delivery and demand
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: There are different classifications (some classify obstructive shock as a subset of cardiogenic shock)
Notes: In any type of SHOCK tissue perfusion is determined by MAP - which is used as a measure of perfusion (MAP as a measure of perfusion is only a surrogate measure, and is not 100% accurate - however sometimes it’s all we have to go by)
MAP = cardiac output multiplied by systemic vascular resistance = 2/3 systolic + 1/3 diastolic
SVR is governed by the vessel length, blood viscosity, and vessel diameter
CO = heart rate (HR) multiplied by Stroke Volume (SV)
Notes:
Cardiogenic shock is a shock state that occurs as a consequence of cardiac pump failure, resulting in decreased cardiac output (CO). Pump failure can occur both as a result of an abnormality of the Heart rate or the Stroke volume
Notes:
-BaroRc sense the decreased cardiac output and leads to increased SVR in an effort to compensate for the diminished CO
-The vasoconstrictive mechanisms (I.e. the increase in systemic vascular resistance) compensate for decreased tissue perfusion by redirecting blood from the periphery to the vital organs, thereby maintaining coronary, cerebral, and splanchnic perfusion.
Instructions: Ask the learner what are some causes of Cardiogenic Shock. Answer is provided in the slide
Notes: Myocardial infarction causes cardiogenic shock when greater than 40 percent of the left ventricular myocardium is involved or when right ventricular infarction leads to decreased preload
Notes: If the blood outflow from the heart is decreased because there is decreased return to the heart (due to an obstruction) or “obstructed” as the blood leaves the heart the stroke volume diminishes, with the overall effect of decreasing the cardiac output
Notes:
-Again the BaroRc sense the decreased cardiac output and lead to increased SVR in an effort to compensate for the diminished CO
-The vasoconstrictive mechanisms (I.e. the increase in systemic vascular resistance) compensate for decreased tissue perfusion by redirecting blood from the periphery to the vital organs, thereby maintaining coronary, cerebral, and splanchnic perfusion.
Instructions: Ask the learner what are some causes of Obstructive Shock. Answer is provided in the slide
Notes:
-Hypovolemic shock is a consequence of decreased preload due to intravascular volume loss.
-The decreased preload diminishes stroke volume, resulting in decreased cardiac output (CO).
Notes:
-Again the BaroRc sense the decreased cardiac output and lead to increased SVR in an effort to compensate for the diminished CO
-The vasoconstrictive mechanisms (I.e. the increase in systemic vascular resistance) compensate for decreased tissue perfusion by redirecting blood from the periphery to the vital organs, thereby maintaining coronary, cerebral, and splanchnic perfusion.
Instructions: Ask the learner what are some causes of Hypovolemic Shock. Answer is provided in the slide
Notes: Distributive (vasodilatory) shock is a consequence of severely decreased SVR.
Notes: The cardiac output (with increases in both heart rate and stroke volume) is typically increased in an effort to compensate for the diminished SVR
Instructions: Ask the learner what are some causes of Distributive Shock. Answer is provided in the slide
Notes:
In inflammatory cascade the SVR may initially increase to compensate for leaky vessels (third spacing), but eventually to the inflammatory cascade the SVR decreases
In anaphylaxis the SVR may initially increase to compensate for leaky vessels (third spacing), but eventually to the inflammatory cascade the SVR decreases
Neurogenic shock occurs when injuries to the spine occur above T6 leading to a disruption in the sympathetic chain and therefore decrease vascular tone
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
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:
To determine if we are dealing with shock, there are a few tools at our disposal. The most important are the signs and symptoms.
i.e look for cardinal findings. Laboratory and hemodynamic measures can also help us, however these are often not available. Which
underscores the importance of being able to identify shock early with our clinical history and physical.
Slides 32-35 describe the signs and symptoms associated with pre-shock and shock
Notes: Change in mental status — The continuum of mental status changes frequently encountered in shock begins with agitation, progresses to confusion or delirium, and ends in obtundation or coma.
Notes:
Answer to “What are a few exceptions to tachycardia?”
-neurogenic shock
-relative tachycardia - e.g. in an athlete HR of 90 is tachycardia
-bradycardic causes of shock!
-bradycardia in severe shock - an agonal event from any cause of shock
Notes:
Tachypnea occurs due to two reasons
-Chemoreceptors sense hypoxia and compensate by causing tachypnea
-Also tachypnea is a compensatory mechanism for metabolic acidosis (to blow off CO2)
Notes: In a patient who is hypertensive at baseline, 40 mmHg drop in systolic BP is technically hypotension = relative hypotension
Notes:
-Vasoconstriction causes the cool and clammy skin that is typical of shock. Not all patients with shock have cool and clammy skin, however. Patients with early distributive shock or terminal shock may have flushed, hyperemic skin. The former occurs prior to the onset of compensatory vasoconstriction, while the latter is due to failure of compensatory vasoconstriction.
-In most settings of shock (other than early distributive shock) there will be decreased capillary refill
-Oliguria — Oliguria may be due to shunting of renal blood flow to other vital organs, intravascular volume depletion, or both. When intravascular volume depletion is a cause, it may be accompanied by orthostatic hypotension, poor skin turgor, absent axillary sweat, or dry mucous membranes.
Notes: This is a summary slide
Notes: to standardize the diagnosis of shock, 4 of these 6 criteria have to be met to define shock
Notes:
Lactate is increased due to:
-Decreased O2 --&gt; aerobic metabolism switches over to anaerobic --&gt; byproduct = lactate
-Decreased hepatic clearance
Metabolic acidosis — Metabolic acidosis develops as shock progresses, reflecting decreased clearance of lactate by the liver, kidneys, and skeletal muscle.. Lactate production may increase due to anaerobic metabolism if shock progresses to circulatory failure and tissue hypoxia, which can worsen the acidemia
Notes:
In one pediatric study - death occurred in 16% with no early treatment versus 5% with early treatment.
Reference: Carcillo et al. Crit Care Med 2002;30;1365
Notes: i.e. ABC’s should be done within 5-15 minutes
Notes:
Quickly reversible causes - examples = reverse tachyarrhythmia with meds, anaphylaxis than responds quickly to epinephrine
Inability to oxygenate - examples = cardiogenic shock leading to pulmonary edema, ARDS
Inability to maintain airway - examples = upper airway obstruction due to anaphylaxis or trauma
Work of breathing - examples =
-in pt with sepsis or cardiogenic shock by eliminating the work of breathing can take a load off the metabolic/hemodynamic stressors, which can lead to improvement of shock
-Also if the work of breathing is suggesting that there is impending respiratory fatigue, intubate
Choose intubating agent carefully
- etomidate, midazolam, fentanyl cause less cardiovascular depression than other agents.
-ketamine can be useful as it maintains cardiovascular status (in fact it leads to increased HR and blood pressure)
-if have no other agents titrate benzodiazepines
-Avoid propofol, thiopental
Notes:
-Ongoing fluid resuscitation past the 3 boluses is based on maintaining urine output 1-2 ml/kg/hr
-With large volumes of NS (&gt; 4L) can develop a normal anion gap (hyperchloremic) acidosis - may consider switching to Ringer’s Lactate
Notes: Crystalloid vs. colloid?
-No benefit to colloids = Clinical trials have failed to consistently demonstrate a difference between colloid and crystalloid in the treatment of septic shock
(ie. no mortality or clinical outcome difference). Colloids are significantly more expensive than crystalloids.
Crystalloid versus colloid trials =
-SAFE trial - 4% albumin - no difference in 28 day mortality - Finfer et al NEJM 2004;350:2247
-VISEP trial - pentastarch - no difference in 28 d mortality but a trend toward increased
90 d mortality with pentastarch (stopped early) - Brunkhorst et al NEJM 2008;358:125
Notes: This slide discusses the choices of vasorpessors and inotropes available
-Dopamine has fallen out of favour as the vasopressor of choice in cardiogenic shock
-Dobutamine 2-10 micrograms/kg/minute +/- Norephinephrine 0.01-3 micrograms/kg/minute (usual range 8-30 micrograms/minute)
-Epi and Dopamine likely not a good idea - can cause increased HR
De Backer et al N Engl J Med 2010;362;779
-1679 pts with shock (hypovolemic, cardiogenic, septic shock) were randomized to either dopamine or norepinephrine if still hypotensive after fluids
-primary end point was death at 28 days
-Dopamine and NE no difference in mortality when used in all-comers with shock
-however dopamine increased mortality in cardiogenic shock!
-also, significantly more patients on dopamine developed arrythmias (24 vs 12%)
Levy B et al. Crit Care Med 2011 Mar; 39:450.
-small open randomized trial study (approximately 30 pts in each arm) in pts with cardiogenic shock
-norepinephrine/dobutamine versus epinephrine
-10/15 in epi group and 11/15 in NE/D group survived
-epi was associated with significantly mean higher HR and mean lactate level, and new arrythmias were observed in 2 pts in epi group
-small study - therefore hard to draw any conclusions from it
Notes:
Central venous catheter
-can be used to infuse IV fluids quickly, infuse medications, draw blood and hemodynamic monitoring
-hemodynamic monitoring = CVP and central venous O2 saturation (ScvO2)
Pulmonary artery catheters (or Swan Ganz catheter) can measure the pulmonary occlusion pressure (PAOP) and SvO2 (mixed venous oxyHg saturation)
-PAOP has proven to be a poor predictor of fluid responsiveness in sepsis and SvO2 is similar to ScvO2
-also they increase complications without improving outcome - Therefore its use is not recommended = Animation 1-2
…to guide your early directed goal directed therapy
Notes: Remember that a retrospective cohort study of 2124 patients demonstrated that time to initiation of appropriate antibiotic was strongest predictor of mortality - Kumar et al Crit Care Med 2006;34;1589.
