Shock - Types Pathophysiology and

management

Dr.Ravichandra Kumar
Anaesthesia Resident
Definition
• Shock is a state characterized by systemic reduction in tissue perfusion
resulting in decreased tissue oxygen delivery.

• Circulation fails to meet the metabolic need of the tissue & at the same
time fails to remove the metabolic waste products.

• Usually result of inadequate blood flow and/or oxygen delivery.

• Leads to anaerobic metabolism.

Hypovolemic shock
• Due to decreased circulating blood volume in relation to the total
vascular capacity.
• Characterized by a reduction of diastolic filling pressures.
• Causes
Blood loss: trauma
Plasma loss: burns
Water loss: Vomiting, diarrhea, sweating.
Cardiogenic shock

• Cardiac pump failure related to loss of myocardial contractility,

mechanical failure of the cardiac anatomy
• Characterized by elevations of diastolic filling pressures and volumes
• Causes
• Myocardial Infarction
• Cardiac Arrythmias
• Cardiomyopathy
• Valvular Heart Disease
Obstructive shock
• Due to obstruction to flow in the cardiovascular circuit and
characterized by either impairment of diastolic filling or excessive
afterload
Cardiac tamponade
Constrictive pericarditis
Tension pneumothorax.
Massive pulmonary embolism
Aortic stenosis.
Distributive shock
• Caused by loss of vasomotor control resulting in arteriolar/venular
dilatation and characterized by increased cardiac output and decreased
SVR
• Causes
Sepsis
Anaphylactic Shock
Neurogenic
Pathophysiology
MICROVASCULAR PATHOPHYSIOLOGY
• α1 receptors – vasoconstriction
• ẞ2 receptors - vasodilation.
• Shock norepinephrine & epinephrine from adrenal medulla → α1
receptors
• Other constrictors: A-II, vasopressin, endothelin 1, and TxA2
• Vasodilators: PG I2, NO and adenosine
Reversible Stage:
Irreversible State
CVS
• ↓ ↓ Preload & ↓ Afterload
• ↑ sympathetic output
• causes catecholamine release from adrenal medulla.
• ↑ heart rate & contractility venous and arterial vasoconstriction
(Except in sepsis).
• Arterial vasoconstriction with regional variations
• Shunting of blood away from less essential organ beds such as the
intestine, kidney, and skin.
Pulmonary Pathophysiology

• Tachypnea
• ↑ minute ventilation & ↑ CO2 excretion
• Compensatory respiratory alkalosis.
• Resuscitation induced O2 free radical injury
• ALI & ARDS.
• Non cardiogenic pulmonary edema
Renal

• Decreased renal blood flow.

• RAS activation.
• ↓ GFR + ↑ aldosterone & vasopressin → Oliguria
• Further vasoconstriction → ↑ sodium & water retention → edema
• Toxic tubular injury & Tubular obstruction
Renal
Endocrine Pathophysiology
• Na+ & water retention K+ & H+ lost
• Hypovolaemia ADH
• Adrenergic drive Norepinephrine release
Vasoconstriction.
↑ glycogenolysis & ↑ gluconeogenesis.
↓ Insulin release
Compensated Shock
• Reversible stage during which compensatory mechanisms are effective
and homeostasis is maintained.
• Clinical presentation begins to reflect the body’s response to the
imbalance of oxygen supply and demand.
• At the cellular level from aerobic to anaerobic, causing the lactic acid
build up which is removed by the liver, but needs oxygen
• At this stage, the body is able to compensate for the changes in tissue
perfusion.
• If the underlying cause is corrected, the patient will recover with little to
no residual effects
Cardiovascular
Release of
epinephrine/norepinephrine which
promotes vasoconstriction.
↑contractility
↑heart rate
Coronary artery dilation.
Narrow pulse pressure
BP remains adequate to perfuse
vital organs
Renal
↓renal blood flow
↑renin resulting in release of
angiotensin (vasoconstrictor) ◦
↑aldosterone resulting in sodium
and water re- absorption
↑ antidiuretic hormone
resulting in water re- absorption
• Respiratory
↓blood flow to the lungs
hyperventilation
• Gastrointestinal
↓blood supply and Hypoactive bowel sounds.
• Renal
↓renal blood flow
↑renin resulting in release of angiotensin (vasoconstrictor).
↑aldosterone resulting in sodium and water re-absorption
↑ antidiuretic hormone resulting in water re- absorption
Uncompensated stage
• This stage of shock begins when the body’s compensatory mechanisms
fail.
• Aggressive interventions are need to prevent the development of multiple
organ dysfunction syndrome (MODS).
• Continued decreased cellular perfusion and resulting alerted capillary
permeability are the distinguishing features of this stage.
• Altered capillary permeability allows leakage of fluid and protein out of
the vascular space into the surrounding interstitial space causing a decrease
in circulating volume and an increase in systemic interstitial edema.
• This fluid leak from the vascular space also affects the solid organs
 Irreversible Shock
• Decreased perfusion from peripheral vasoconstriction and decreased
cardiac output exacerbate anaerobic metabolism.
• Lactic acid accumulates and contributes to an increased capillary
permeability and dilation of the capillaries.
• Blood pools in the capillary beds secondary to constricted veins and
dilated arteries.
• Loss of intravascular volume leads to worsening of hypotension and
tachycardia resulting in a decrease in coronary blood flow.
• Cerebral blood flow cannot be maintained and cerebral ischemia
Key laboratory findings.
• ↓ blood glucose .
• ↑ ammonia, lactate and potassium.
• Metabolic acidosis
• Renal paremeters will be elevated.
 Septic Shock
• Results from moderate to severe sepsis or tissue damage. It is considered as
part of a spectrum and a progression of SIRS (systemic inflammatory
response syndrome), not responsive to I.V Fluids
• SIRS (systemic inflammatory response syndrome ): Characterized by the
presence of two or more of the following clinical criteria:
Temperature(core) >38°C or<36°C
Heart rate > 90beats/min
Respiratory rate >20/min or PaC02 <32mmHg
WBC >12000cells/ml or <4000cells/ml or >10% immature
band forms.
Risk Factors
• Age (<10 and >70years)
• Malnutrition,
• Anemia,
• Primary disease: Malignancies, DM, CLD, CRF
• Immunosuppression,
• Indwelling catheters
• Prolonged hospitalisation
• Major surgeries, trauma, extensive burns
Pathogenesis
• Micro-organisms or products of tissue damage stimulates production of pro-
inflammatory cytokines which in turn stimulate production of secondary
mediators of inflammation in order to localize infection and limit
proliferation.

• The production of the pro-inflammatory cytokines is regulated to limit

damage.

• However in poorly controlled sepsis or extensive tissue damage, there is

excessive inflammatory response which is poorly regulated.
• Secondary mediators of inflammation (Kinins, IL-1,IL-6, oxygen free
radical, proteases.)
• Effects of secondary mediators
Damage of vascular endothelium
Vasodilation of microvasculature
Activation of neutrophils(aggravates endothelial damage)
Diminished force of cardiac contraction

• These ultimately lead to peripheral pooling of blood, extravasation of

fluid, hypotension, hypoxia and shock
• Effect of compliment activation
Vasodilatation and increase permeability
Endothelial damage
C5a causes aggregation of platelet and leucocytes thereby acting
as procoagulant leading to DIC.

• Pro-inflammatory cytokines reduces plasma levels of

thrombomodulin, coagulation inhibitors like protein S, protein C, and
ATIII. Microvascular coagulation results which worsens DIC.
EARLY STAGE
Not associated with hypovolemia, compensated/warm shock
Febrile (38.2-41°C)
Shivering and malaise
Warm dry and flushed skin.
Hyperventilation
Rapid bounding pulse
Wide pulse pressure
Late Stage Decompensated
Hypovolemia with superimposed sepsis, cold shock
Altered sensorium
Cold clammy skin
Feeble pulse
Hypothermia, hypotension
Oliguria
Upper GI bleeding
DIC
Management
• Systemic examination is done to detect any focus of sepsis
• Investigation goes hand-in-hand with resuscitation
• There is leucocytosis after initial leucopenia, Throbocytopenia.
• Septic work up
Blood culture
Sputum c/s
Urine c/s
Wound swab c/s
• Based on suspected source (CXR, Abd-X RAY, Abd-pelvic USG, CT
Scan of various sites)
SOFA
• Sequential organ failure assessment
• Sepsis related organ failure assessment because it was initially
developed in 1994 to describe the degree of organ dysfunction
associated with sepsis patients.
• Score involves six organ systems - RS, CVS, Renal, Hepatic, CNS
and Coagulation.
• Function of each system is given a score of 0 to 4.
• Higher the score higher the mortality.
 Respiratory rate ≥22/min
Altered mentation
Systolic blood pressure
≤100 mm Hg

Non-ICU patients with qSOFA = 2-3 are at increased

risk of death or prolonged ICU stay (> 3 days)
 Surviving Sepsis Campaign 2018

• “The most important change in the revision of the SSC

bundles is that the 3-h and 6-h bundles have been
combined into a single “1-hour bundle” with the
explicit intention of beginning resuscitation and
management immediately.”
Treatment
• Septic shock is a medical emergency that requires prompt and efficient
resuscitation
• Patient should be admitted to ICU.
• AIM
Improve haemodynamic state
Restore tissue perfusion thereby increase O2 tissue.
Administer O2
Combat the bacteria and cytokines
Eliminate septic focus
• VOLUME REPLACEMENT

IV access with 2 wide bore cannulas are secured, samples taken.

Crystalloids started: 500 ml to 1L in 30 mins Then re-assess, and
repeat as appropriate.
Urethral catheter is passed to empty the bladder then to monitor the
hourly urine output
Central venous catheter is inserted
Vasopressors to maintain MAP > 65mmH
Norepinephrine is 1st line of choice if unresponsive to Fluids
• OXYGEN ADMISTRATION
In a cleared and patent airway, O2 is delivered via a face mask to
increase O2 saturation. Increasing uptake and delivery to tissue.

• ANTIBIOTIC
Large doses IV to combat infection.
Empirical IV Broad spectrum bactericidal & anaerobe coverage.

• STEROIDS:
Inhibits conversion of membrane phospholipid to arachidonic acid
hence inhibiting release of secondary mediators.
• NSAIDS
Inhibits the COX pathway there by PG and TBX synthesis
Prevent neutrophil aggregation and activation
↓production of superoxide radicals
Stabilizes lysozomal membranes enzymes.

O2 Free radical scavengers

Superoxide dismutase
Vitamin C, allopurinol, α-tocopherol
They have been shown to decrease tissue damage and MOD in septic
shock if given prophylactically.
.
Poor Prognosis

• Advanced age
• Immunosuppresion
• Infection with resistance organism, level of IL -6
• Need for inotrophs for > 24hrs
• Mods despite treatment
Haemorrhagic Shock
• m/c cause in shock in Trauma and Surgeries.
• Compensated upto 15% of volume loss
• Clinical Features
Agitation
Cold clammy extremities.
Tachycardia, Hypotension
Pallor
Weak or absent peripheral pulses
Prolonged capillary refill time
• Investigations
Hematological & Biochemical Investigations.
Lactate levels.
Blood grouping & cross matching.
Radiological investigations – Xrays, FAST.
• Damage control resuscitation.
Permissive hypotension.
Use of limited crystalloids and blood products.
Anticipate and treat coagulopathy.
Hypothermia.
• Dynamic Fluid Response
To determine shock status.
250-500ml bolus over 5-10min.
HR, BP & CVP are measured.

• Hemorrhagic shock Responders

Sustained improvement in CVS status after bolus.
No active bleeding, require fluids to attain normal volume status
• Transient Responders
Initial improvement followed by reverting to previous state over
10-20 min.
Moderate ongoing fluid losses

• Non responders.
No improvement in CVS status following bolus.
Severely volume depleted and likely to have ongoing loss(persistent
uncontrolled Hemorrhage)
• Transfusion of blood and blood products.
Blood product - PRBC Hb 7-9 gm/dl
Coagulation factor-based products
Platelets > 50,000/ml.

Monitoring Response
NIBP
Urine output
Pulse oximetry
CVP.
Invasive BP monitoring
Base deficit & serum lactate
End Point of Resuscitation
Cardiogenic Shock

• Characterised by primary decrease in cardiac contractability which

results in decrease in Ventricular output

• SBP < 80 mmHg

• Cardiac Index <2 litre/min/m2
• LVEDP or PCWP > 18 mmHg
• MAP is 30 mmHg below the basal values
Etiology
Clinical Features
Circulatory Insuffiency

Circulatory Congestion
• Diagnosis.
ECG to look for ischemic changes
ECHO for ventricular function
Cardiac Filling pressures
CXR
ABG
Cardiac enzymes.
Invasive monitoring
 Management
Aim – Increase Cardiac Output,
Improve Coronary Blood Flow
Reduce Transdution of Fluid into Lungs
IAB
P
Obstructive Shock
Associated with physical obstruction of the great vessels or the heart
Thank You