Overwiew of Shock

Ijir A
Hypotension

Circulatory Failure

Shock
Definition

• Shock is a physiologic state of inadequate tissue perfusion with

impaired oxygen delivery and/or utilization, resulting in cellular and
tissue hypoxia, which disrupts normal cellular function and
metabolism.

• Shock is a severe/ life-threatening manifestation of circulatory failure

• "Shock is typically (but not always) accompanied by hypotension."

Shock

• The consequence of shock is cellular and tissue hypoxia and ultimately

cellular death and organ dysfunction

• Initially reversible, but must be recognized and treated immediately

to prevent progression to irreversible organ dysfunction including
MODs and death
Stages of Shock - A progressive process: Intervene early

Pre shock (Compensated Shock):

• Cardiac output (HR x SV) and systemic vascular resistance (peripheral vasoconstriction)
work to keep BP within normal

Hypotensive (Uncompensated) Shock:

• Compensatory mechanisms are overwhelmed
• most of the classic signs and symptoms of shock appear due to early organ dysfunction

Irreversible Shock:
• Irreversible organ damage, cardiac arrest, death occur.
Stages of Shock - A progressive process: Intervene early
Shock
• Inadequate perfusion to meet tissue demands. A progressive process.

• In other words, a systemic reduction in tissue perfusion  decreased tissue

O2 delivery.
• A shift to less-efficient anaerobic metabolism, leading to lactic acidosis, occurs.

• Initially, effects are reversible. Eventually:

• Cell membrane ion pump dysfunction
• Cellular edema, leakage of cells’ contents
• Inadequate regulation of intracellular pH
•  Cell death, organ failure, cardiac arrest, and death.
Recognizing shock

• There is no single exam or lab test that is sensitive or specific enough

to serve as the gold standard for diagnosing shock.

• Diagnosis should be based on the overall clinical impression,

incorporating a wide range of physical findings and laboratory

abnormalities.
 Recognizing shock
• Low blood pressure is one of the most common
findings in shock, but it is not universally present.

• Patients in shock may be:

• Hypotensive (low blood pressure)

• Normotensive (normal blood pressure)

• Hypertensive (high blood pressure)

• Not all hypotensive patients are in shock—

hypotension alone is not diagnostic.

• The most important marker of impaired tissue

perfusion is elevated lactate levels
Other features – depends on type of shock

• Dry mucous membranes

• Chest pain

• Fever/rigors

• Angioedema/urticaria
Physiology of Shock
• The circulatory system can be likened
to an electrical circuit

• Battery – maintains electrical potential

gradient – voltage

• Wire – transmits current between

points of different electrical potential

• Resistor
Physiology of Shock

Because CVP is usually at or near 0 mmHg, this relationship is

often simplified to: MAP ≈ CO × SVR
Determinants of Perfusion pressure

• Perfusion pressure = CO × SVR

• Perfusion pressure = SV × HR x SVR

• Stroke volume is dependent on

• Preload

• Contractility
Determinants of Perfusion pressure

• Perfusion pressure = CO × SVR

• Perfusion pressure = SV × HR x SVR

• Stroke volume is dependent on

• Preload

• Contractility
Determinants of Perfusion pressure

• Therefore low perfusion pressure (shock) must be due to one of the

following
• Low preload

• Low contractility
• Low HR

• Low SVR
Classification of Shock
Type of Shock Primary Physiologic Derangement Common Etiologies

Hypovolemic Shock Low preload Hemorrhage, vomiting, diarrhea

(due to loss of intravascular
volume)

Cardiogenic Shock Decreased contractility (CO) Myocardial infarction, heart failure,

myocarditis

Distributive Shock Decreased SVR Sepsis, anaphylaxis, neurogenic

(vasodilatory) shock, adrenal insufficiency.

Obstructive Shock Decreased preload Pulmonary embolism, tension

(due to obstruction of venous pneumothorax, cardiac tamponade.
return to the LV)
Other distinctive forms of shock...

• “Arrhythmoenic Shock”
• Low HR

• High HR – causing low preload due to short diastolic filling time

• Often classified as a form of cardiogenic shock

• “Toxin mediated shock” eg cyanide and carbon monoxide poisioning

Classifications of Shock
o Hypovolemic Shock o Cardiogenic Shock
o Decreased preload due to
o “Pump failure.”  CO, systolic
internal or external losses.
function.

o Distributive Shock
o Obstructive Shock
o Decrease in SVR, with abnormal
distribution of blood flow  o Outflow from left or right side
functional hypovolemia, of heart physically obstructed.
decreased preload.
o Typically, NL or  CO.
Hypovolemic
• Hypovolemic shock is characterized by
decreased intravascular volume and increased
systemic venous assistance (compensatory the
mechanism to maintain perfusion in the early
stages of shock)

• In the later stages of shock due to progressive

volume depletion, cardiac output also
decreases and manifest as hypotension.

• Hypovolemic: hemorrhagic and non-

hemorrhagic
Cardiogenic

• Pump failure leading to

decreased cardiac output and
systemic hypoperfusion
• Causes can be divided into 4
main categeories
Obstructive

• Mostly due to extracardiac

causes
• Outflow from left or right side of
heart physically obstructed
• Leading to a decrease in the left
ventricular cardiac output
• Pulmonary vasculature or
mechanical
Distributive
• Characterized by peripheral
vasodilatation
• Types
• Septic shock
• Anaphylactic shock
• Neurogenic
• Endocrine - adrenal failure
(Addisonian crisis), myxoedema
Recognising the type of shock

• Sometimes easy but can also be very challenging

• Requires knowledge of hemodynamic parameters

• Limitations requires integrating clinical assessment and imaging

parameters
Recognising the type of shock -classic
hemodynamic profiles

This description is not practical clinically

Limitations
• Invasive Monitoring Limitations:
• Central venous and pulmonary artery catheters may not always be available or
accurate.
• Dynamic Nature of Shock:
• Shock states evolve over time; classic profiles assume fixed states.
• Example: Early septic shock → high cardiac output (CO), late septic shock
→ low CO.
• Hypovolemic shock may begin with normal CO/CVP but deteriorates as
volume loss progresses
Limitations
• Overlap Between Shock Types:
• Different shock types can share features as they progress:
• Septic shock (distributive) → myocardial depression → cardiogenic
features.
• Obstructive shock → elevated CVP, mimicking cardiogenic shock
• Patient Variability:
• Chronic conditions (heart failure, hypertension) alter baseline values (e.g.,
chronically high CVP).
• Compensatory mechanisms may temporarily mask typical shock features.
Limitations

• To overcome these drawbacks, clinicians often integrate bedside

assessments and imaging with the classic profiles for a more
comprehensive evaluation of shock.
Limitations
Investigations
• Resuscitation should not delay while investigating the etiology of
undifferentiated shock

• FBC, renal and liver function test, cardiac biomarkers, D-dimer level,
coagulation profile, GXM for a possible blood transfusion if appropriate (if
concern for haemorrhagic shock), blood and urine cultures, and blood gas
analysis

• CXR
Treatment – General Principles
• While treatment should be aimed at Priorities
the underlying cause of shock, the 1. Pulse, ventilation and oxygenation
most critical aspect of treatment is
2. Fluids (unless in catdiogenic shock)
prompt resuscitation with restoration
of normal hemodynamics 3. Pressors (vasopressor and
inotropes)

4. Other specific mgt/Tx of cause

1 2 3 = Resuscitation
Treatment
Resuscitation
• Immediate treatment with intravenous (IV) fluid should be initiated plus
vasopressor therapy, if needed
• to maintain tissue perfusion
• Avoid IVF in cardiogenic shock or Judicious use of IV fluids in the absence of pulmonary
oedema

specific therapies
• depend on aetiology
Treatment – General Principles
IVF Vasopressors Inotropes
(inc CVP) (inc SVR) (inc contractility)

Hypovolemic + Temporary use only -

Distributive + + +/-

Cardiogenic - +/- +

Obstructive +/- +/- +/-

Specific Tx

• Hypovolemic
• Aggressive IV fluid resuscitation with 2 to 4 L of isotonic crystalloids

• Blood transfusion if haemorrhagic

• Treat underlying cause

• Use vasopressors if needed

 Specific Tx Goal MAP 65mmHG

• Cardiogenic
Fluids – access vol status
+/- small fluid trial (250-500 ml) or passive leg raise

BP support - Pressor

Dopamine (5-15 mcg/kg/min)

Norepi (0.03 – 0.3 mcg/kg/min)

Inotrope
Dobutamine (5-20 mcg/kg/min)
Milrinone (0.375 – 0.75mcg/kg/min) BP
Choice of vasoactive substance not clear cut
Specific Tx
• Others
• MCS e.g IABP IMPELLA ECMO
• Augment co
• Reduce myocardial workload and O2 demand
• Improve BP
• Serve as a bridge
• Bipap or Mech vent
• decreases workload and also pushes fluid out of the
lung
• Optimize O2 carrying capacity of blood
• Treat cause
• HF
• STEMI - thrombolysis or PCI
• Cardioversion – for unstable tachyarrhythmia or
bradyarrhythmia
Specific Tx

• Septic –

• initial aggressive fluid resuscitation with IV isotonic crystalloids 30 mL/kg within

3 hrs with additional fluid based on frequent reassessment

• Empiric antibiotic therapy

• Vasopressors if needed (target a mean arterial pressure (MAP) of 65 mmHg)

• Norepinephrine – first choice with the addition of vasopressin if refractory

Specific Tx

• Anaphylactic shock
• aggressive IV fluid resuscitation with 4 to 6 L of IV crystalloids

• Stop the offending agent

• intramuscular epinephrine

• Antihistamines

• Corticosteroids

• nebulized albuterol
Specific Tx
• In adrenal crisis
• judicious fluid resuscitation
• IV dexamethasone
• Obstructive
• judicious fluid resuscitation
• Massive PE – thrombolysis
• Tension pneumothorax - needle thoracotomy followed by tube thoracotomy
3 Principles related to diagnosis of shock
• Not all patients with shock have hypotension
... And not all hypotensive patients have shock

• Determining type of shock should never be based on just one parameter but
should incoporate as much data as possible

• More than one type of shock may coexist in same patient

• Sepsis + hypovolemic
• Sepsis + sepsis induced cardiomyopathy
Prognosis

• Sepsis and septic shock, in general, are associated with long-term

morbidity and mortality, with many of the survivors requiring
placement into long-term acute care facilities or post-acute care
centers

• Hypovolemic and obstructive shock generally have much lower

mortality and respond better to timely treatment
Cardiogenic Shock
Definition
Clinical
• Poor cardiac output state and evidence of tissue hypoxia due to
cardiac dysfunction in the presence of adequate intravascular pressure
and left ventriculuar filling pressure
Hemodynamic
• Persistent hypotension for at least 30 minutes with depressed cardiac
index in the presence of adequate or elevated filling pressure
Reduced Mortality - Evolution
• Historically, mortality for
cardiogenic shock had been 80% –
90%
• Recent data indicate that the rate
has dropped to 40% – 50% due to
better therapies, the advent of
thrombolytics, improved
interventional procedures.
Staging - SCAI
Causes
• Ischemic vs Non Ischemic
• Ischemic cardiogenic shock is
more common
• Acute coronary syndrome is the
most common cause of CS
• Acute on chronic HF execebation
in the setting of ischemic or non
ischemic CM – also common
cause
Berg et al Cardiovasc Qual Outcomes 2019
Cardiogenic shock phenotypes

• facilitates risk stratification

• tailor patient-specific
management strategies

• improve outcomes
Multidisciplinary approach
• Advent of shock teams
• Shock teams likely improve patient outcomes by facilitating early patient
phenotyping and appropriate intervention
Vasoactive treatment strategy
• Choice of vasoactive therapy is not
clear cut

• Either has not been shown to be

superior

• Most important thing is to be able

to identify shock early, initiate
therapy
Bloom JE et al