2. What is Shock?
• SAMUEL V GROSS, 1872 said - “Shock is the manifestation of the
rude unhinging of the machinery of life”
• Shock is a state of acute circulatory insufficiency that creates an
imbalance between tissue oxygen supply (delivery) and oxygen
demand (consumption) resulting in end-organ dysfunction
• A clinical syndrome that results from inadequate tissue perfusion
• Failure of circulation centrally or peripherally to meet the
metabolic demands of the tissues
• A group of life-threatening circulatory syndromes with varying
physiological profiles.
5. HYPOVOLEMIC SHOCK
A decrease in circulating volume in relation to
the total vascular capacity and characterized by a
reduction of diastolic filling pressures resulting in
poor tissue perfusion. Commonest cause being
trauma resulting in external or concealed
haemorrhage from blunt or penetrating injuries.
6. ETIOLOGY
Hemorrhagic shock - severe blood loss leads to inadequate
oxygen delivery at the cellular level.
Traumatic
1. Blunt or penetrating injury
2. Fractures- long bones, pelvic fractures
Non- Traumatic
1. GI bleeds
2. Aortic dissection
3. Rupture of large vessel aneurysm
4. Erosion of a large vessel
5. Diffuse inflammation of mucosal surfaces
7. Due to loss of water and electrolytes, with fall in
effective circulating volume.
Traumatic
i. Burns
ii. Crush injuries
Non-traumatic
i. Fluid loss from vomiting or diarrhoea (eg- cholera)
ii. Fluid loss in diabetes mellitus, adrenal insufficiency,
excessive sweating, diabetes insipidus
iii. Fluid sequestration (eg- intestinal obstruction,
pancreatitis)
ETIOLOGY
8. PATHOPHYSIOLOGY
Ventricular preload - DBP and volume
Decreased SV and CO, hence SBP
CO leads to SVR to maintain perfusion to heart and
brain at the expense of other tissues ( muscle, skin, gut)
Autoregulation occurs at heart and brain- maintenance
of blood flow over wide range of perfusion pressure
(60- 150mm of Hg).
Circulating
volume
Venous
return
Right and
left filling
pressures
Cardiac
output
Tissue
hypoxemia
9. Neurohumoral Compensatory Mechanisms-
1. Catecholamines
2. Cortisol
3. ADH secretion
4. RAS activation
Shift of fluid from extravascular compartment to
vascular compartment
1. PHASE 1- <1 hr of blood loss, shift from interstitium to
capillaries (may continue upto 40hrs)
2. PHASE 2- RAS activation- Na+ and water retention to
replenish interstitial fluid
3. PHASE 3- Erythropoesis.
PATHOPHYSIOLOGY
10. DETERMINANTS
Arterial oxygen content
CaO2 = (1.39 x Hb x SaO2) + (PaO2 x 0.0031)
Oxygen delivery= Cardiac Output x Arterial O2 content
DO2= CO x [(1.39 x Hb x SaO2) + (PaO2 x 0.0031)]
Oxygen consumption= Cardiac Output x (Arterial O2
content- Venous O2 content)
Vo2= CO x (CaO2- CvO2)
= CO x Hb x 1.39 ( SaO2- SmvO2)
11. MICROVASCULATURE
• Impairment of microcirculation- central pathophysiology
of shock
• Imbalance between vasoconstrictors (Angiotensin II,
endothelin-1, thromboxane A2) and vasodilators (PGI2,
NO, adenosine)
CELLULAR RESPONSE
Increased
anaerobic
metabolism
lactate, H+ ion
accumulation
Acidosis
Decrease in interstitial transportation of
nutrients
Mitochondrial dysfunction- decreased oxidative
phosphorylation
Decrease in ATP store
12. ORGAN RESPONSE
Endocrine
1. Increased gluconeogenesis and lipolysis.
2. In critically ill, cortisol levels and ACTH stimulation is
decreased, hence survival rates are low.
3. Pancreas- increased secretion of glucagon- increased
gluconeogenesis increasing blood glucose levels.
Renal Response
1. Decreased urine output
2. Hypoperfusion – AKI
3. Acute tubular necrosis
Severe pain/stress ACTH stimulation Cortisol secretion
Reduced
RBF Reduces
GFR
Reduced
U/O
Aldosterone
Vasopressin
13. ORGAN RESPONSE
Cardiovascular response
1. Hypovolemia preload SV
2. HR CO(limited)
3. Venoconstriction
4. Shock induced decreased myocardial filling causes
decrease in LV end-diastolic volume and fall in SV
5. Hypothermia, myocardial ischemia and acedemia
impairs myocardial contractility and SV.
6. Shock Index, SI= HR/SBP (normal= 0.5-0.7)
14. Pulmonary Response
ORGAN RESPONSE
SHOCK
Increased PVR
PVR> SVR it may lead to RV failure
Tachypnoea (reduced TV, high RR)
Respiratory Alkalosis
15.
16. HAEMORRHAGIC SHOCK
Definition of Massive Haemorrhage
1. Loss of more than one volume of blood in 24hrs
2. 50% total blood volume lost in 3hrs
3. Bleeding in excess of 150mL/min
17.
18. How does a patient present?
Clinical Features:
1. Pallor
2. Slight anxiety/ restlessness
3. Cold, clammy skin
4. Tachycardia
5. Collapsed neck veins
6. Oliguria (<0.5ml/kg/hr) or anuria
“Any patient who is cool and tachycardic is in shock
until proven otherwise”(ATLS)
20. Factors STAGE I STAGE II STAGE III STAGE IV
Blood loss (mL) 750 750-1500 1500-2000 2000 or more
Blood loss (% blood
volume)
15 15-30 30-40 40 or more
Pulse (beats/min) <100 >100 >120 140 or higher
Blood pressure Normal Orthostatic Decreased Decreased
Pulse pressure (mm Hg) Normal or increased Decreased Decreased Decreased
Capillary refill test Normal Positive Positive Positive
Respirations per minute 14-20 20-30 30-40 >40
Urine output (mL/hr) 30 20-30 <20 Negligible
CNS: mental status normal anxious Anxious, confused
Confused,
lethargic
Fluid replacement Crystalloid Crystalloid Crystalloid + blood
Crystalloid +
blood
Baskett’s Classification of Haemorrhagic Shock
21. Vitals (PR, BP, RR, temp)
Urine output, capillary refill time, JVP, ABG
Hematocrit
Classic hemodynamic pattern- low CVP, low PCWP, low
CO and high SVR.
Oxygen extraction
ETCO2
SaO2 SvO2 O2 extraction
(SaO2-SvO2)
Normal >95% 65-70% ~30%
Hypovolemic >95% 50-65% 30-50%
Shock >95% <50% >50%
Monitoring a case of hypovolemic shock
22. Bedside USG- assess right-sided filling pressures,
IVC diameter and caval index
The Rapid Ultrasound in Shock (RUSH) exam
involves a threepart bedside physiologic
assessment simplified as
1. the pump (cardiac),
2. the tank (volume status)
3. and the pipes (arterial and venous)
23.
24. MANAGEMENT
Fluid Resuscitation- Restoring volume is the keystone
VO2= COx Hb x 1.39 x (SaO2- SvO2)
Fluid challenge- 500 or 1000mL NS rapidly infused over 20min
and reassess the patient after each bolus
Cannulation Site
Catheter Dimensions and relation to flow rate
Infusion Device Length (inches) Flow rate (mL/min)
Peripheral
14G catheter 2 195
16G catheter 2 150
Central
16G catheter 5.5 91
16G catheter 12 54
25. Relation to fluid viscosity and flow rate
Estimating volume requirement
Male 65ml/kg ; Female 60ml/kg
Volume is replaced by calculating the volume deficit
crystalloids in 3:1 ratio and colloids and blood at 1:1 ratio
Fluid Flow rate
(mL/min)*
Crystalloids 100
5% albumin 100
Whole blood 65
Packed cells 20
27. MASSIVE TRANSFUSION PROTOCOL
STEP 1- CONTROL BLEEDING
• Minimise time between arrival and surgery if indicated –
“Damage Control Surgery”
• Use of tourniquet , tamponade techniques, drugs
STEP 2- IDENTIFY THE NEED FOR MASSIVE
TRANSFUSION
• ABC score (4points)
• TASH score (6points)
• Identify massive trauma / bleed on purely clinical basis
• Based on volume requirements after an initial resuscitation.
29. STEP 6: CONSIDER OTHER AGENTS FOR PREVENTION /
LIMITATION OF COAGULOPATHY
Obstetric haemorrhage: early use of cryoprecipitate is
recommended. Platelets: only recommended in
thrombocytopenia < 50,000. Tranexamic acid: give 1 g
loading dose (over 10 mins)
STEP 7:TARGET THERAPY TO RESULTS
• if Hb < 8g/dL- PCV ; if INR > 1.5 or APPT > 50 sec- 2U FFP; if
fibrinogen < 1.0 g/dL - 8U of CP
• Calcium is < 1.1mmol then, 1 amp of Calcium gluconate
1g/10ml
• Maintain temperature > 35 degrees
STEP 8: EVACUATION PLANNING
33. CASE SCENARIO
A 20yr old female, C/O primigravida, with h/o ammenorrhoea of 22 weeks
with severe abdominal pain. Patient had tachycardia with low BP, with
severe generalised pallor. UPT+, B-Hcg+. USG abdomen revealed normal
ovaries, no gestational sac seen in the uterus with moderate to severe fluid
collection seen in abdomen and pelvis.
Patients was immediately taken up for emergency exploratory laparotomy
for suspected ruptured ectopic pregnancy with hemoperitoneum.
On PAC, patient was in obvious distress. PR-130bpm, regular in rhythm, of
low volume, BP-86/66 mmHg in supine position with severe pallor. Airway
examination she had adequate mouth opening
Pre-op tests- Hb-2.7g/dL, TC-25300 cells/cumm, plt-2.96 lakhs/cumm and
PT and INR were normal
34. Anaesthetic management
Plan of anaesthesia- GA
Informed consent - risk of bleeding, multiple blood transfusions, general
anaesthesia related complications
Two wide bore 16 or 18G IV lines.
Standard monitors- PR, BP, SpO2, ECG
Invasive monitors like CVP line & arterial line
Premed- Inj Ranitidine 50mg, Ing Metaclopromide 10mg, Inj. Glycopyrolate
0.2 mg and Inj Fentanyl 2mcg/kg.
RSI with Inj Ketamine 1-2mg/kg and Inj Succinylcholine 2mg/kg
Maintenance- Isoflurane and intermittent boluses of fentanyl. NDMB-
Atracurium 0.5mg/kg
Fluid resuscitation- RL, Colloids, NS; use of fluid warmer to avoid
hypothermia; Vasopressors
Blood components- PRBC, FFP at 1:1 ratio; Inj. Calcium gluconate
Intra-op ABG- correction accordingly
Watch endpoints ; Prolonged surgery- ICU with post op monitoring
35. CARDIOGENIC SHOCK
“Cardiogenic shock (CS) is a low-cardiac-output state
resulting in life-threatening end-organ hypoperfusion
and hypoxia”
Cardiogenic shock is defined as sustained hypotension
with tissue hypoperfusion in spite of adequate left
ventricular filling pressure.
37. EPIDEMIOLOGY
Incidence of cardiogenic shock after an acute MI
varies from 5-19%
In 60% patients, shock develops <48hrs and in
about 30% it occurred >4days after MI.
It carries mortality of over 80%.
LV failure accounts for ~80% cases of cardiogenic
shock complicating acute MI. Acute severe MR,
ventricular septal rupture, predominant RV failure,
free wall rupture or tamponade account for the
remainder.
38. ETIOLOGY
MYOPATHIC
• Acute myocardial
infarction
• Myocardial contusion
(trauma)
• Acute myocarditis
• Cardiomyopathy
• Post-ischemic
myocardial stunning
• Septic myocardial
depression
• Pharmacologic-
Anthracycline toxicity,
Calcium channel
blockers
MECHANICAL
• Valvular failure
(stenotic or
regurgitant)
• Hypertrophic
cardiomyopathy
• Ruptured
interventricular
septum/ ruptured free
wall of ventricle/
ruptured papillary
muscle
OTHERS
• Arrhythmic –
severe tachy or
bradyarrhythmias
• Patients with
myocardial
dysfunction following
open heart surgery
43. Patients at risk of cardiogenic shock following MI
• Proximal obstruction of just LAD artery- infarction of
>40% of LV wall
• Patients with critical three vessel disease
• Acute massive LV infarction
• Inferior wall MI, when it involves RV
• Non- functioning myocardium > critical level (35%)
44. Factors that may trigger or potentiate shock in acute MI
1. Hypovolemia
2. Tachy/brady-arrhythmias
3. Depressant action of drugs- use of propranolol in
early or insidious pump failure, oversedation with
narcotics may induce hypotension
4. Metabolic acidosis, dyselectrolytemia
5. Unrelieved pain
6. Unrelieved hypoxia
7. Pulmonary embolism
45. Refractory chronic heart failure
Reasons why chronic heart failure may decompensate with
cardiogenic shock
Development of new
comorbid condition
Progression of underlying
disease
Infection/sepsis Myocardial ischemia
Renal insufficiency Chronic renal insufficiency
Uncontrolled diabetes Uncontrolled HTN
Anemia
Pulmonary embolism Poor patient compliance with
drug therapy
Hypo/hyperthyroidism
47. Laboratory finding
• CBC, cardiac markers, RFT, LFT, ABG
ECG
Chest X-Ray
Echo – severity of MR, left to right shunt in case of VSR,
evidence of pulmonary embolism
PAC catherization- measurement of filling pressures and
CO
LV catherization and coronary angiography
DIAGNOSIS
48. MANAGEMENT
Principles
1. Improve CO and tissue perfusion
2. Reduce or relieve severe pulmonary edema
3. Maintain a clear airway and a PaO2 of atleast 70mm Hg
4. Correction of electrolyte and acid-base balance
5. Recognize and treat factors which potentiate or
aggravate shock
6. Improve hemodynamic profile
49. Definitive management
Augment cardiac output by one of three ways:
Pharmacological inotropic support
Revascularisation with:
1. Thrombolysis
2. Percutaneous intervention
3. Coronary artery bypass surgery
Intra-aortic balloon counterpulsation
53. Treating Pulmonary Edema
Patients with acute cardiogenic pulmonary edema generally
have an identifiable cause of acute LV failure—such as
arrhythmia, ischemia/infarction, or myocardial
decompensation
SUPPORT OF OXYGENATION AND VENTILATION
• Oxygen Therapy - goal is SpO2 ≥92%
• Positive pressure ventilation- reduces work of breathing,
improves oxygenation.
• Mechanical ventilation- benefits of using PEEP
1. Decreases both preload and afterload
2. Redistributes lung water from the intraalveolar to the extraalveolar space
3. Increases lung volume to avoid atelectasis.
54. Renal Replacement Therapy- Continuous renal
replacement therapy preferred, especially in patients
with hypotension or inotropic support
REDUCTION OF PRELOAD
• Diuretics- furosemide at ≤0.5 mg/kg
• Nitrates - NTG and isosorbide dinitrate. Sublingual NTG (0.4
mg × 3 every 5 min) is first-line therapy for acute cardiogenic
pulmonary edema. If pulmonary edema persists in the
absence of hypotension, it may be followed by IV NTG,
starting at 5–10 μg/min
• Morphine - 2- 4mg IV boluses
• ACE inhibitors- reduce myocardial remodelling
• Other agents- Nestritide, Digitalis Glycosides
55. Anaesthetic considerations
Goals
1. Avoid cardiac depressive drugs (eg- Propofol,
Halothane)
2. Maintain normovolemia
3. Avoid increase in afterload
4. Use of inotropic drugs if required
5. Emergency antiarrhythmic drugs within reach
6. Adequate analgesia
56. Anaesthetic considerations
Detailed history and examination
Informed and written high risk consent
Judicious titration of drugs and fluids in patients
with low ejection fraction
Appropriate premedication
Etomidate- Induction agent of choice
NMDR- Vecuronium
Post-op ICU care
57. OBSTRUCTIVE SHOCK
Obstructive shock or cardiac compressive shock is a low
output state with inadequate perfusion resulting from
compression of the heart and great veins opening into the
right heart causing sharp reduce in diastolic filling.
High intrathoracic pressures- causing compression of the
large veins opening into the right heart and heart
chambers .
59. CLINICAL FEATURES
►Signs of poor peripheral perfusion
►Distended neck veins
►Tension pneumothorax
• Elevated intrapleural pressure collapses intrathoracic great
veins which leads to inadequate venous filling
• Hyperresonant chest,absent breath sounds on affected
site,mediastinum shifted to opposite side
►Displacement of trachea with distended neck veins-
pathognomic sign of tension pneumothorax
61. TREATMENT
Treatment of choice for cardiac
tamponade is pericardial drainage
Tension Pneumothorax- Intercostal chest tube drain
at second ICS.
Pulmonary embolism is usually treated with
systemic anticoagulation, but when massive
pulmonary embolism causes right ventricular failure
and shock, thrombolytic therapy should be strongly
considered.
62. SEPTIC SHOCK
“Sepsis is a life-threatening organ dysfunction caused by a
dysregulated host response to infection.”
Sepsis is a syndrome of physiological, pathological, and
biochemical abnormalities induced by infection.
Septic shock defined as a subset of sepsis in which
profound circulatory, cellular and metabolic
abnormalities are associated with a greater risk of
mortality than with sepsis alone.
63. TERMINOLOGY
Bacteremia: transient invasion of circulation by bacteria
Septicemia: prolonged presence of bacteria in the blood
accompanied by systemic reaction
SIRS (systemic inflammatory response syndrome ): it is a
syndrome characterized by the presence of two or more of
the following clinical criteria:
• Temperature(core) >38°C
• HR>90beats/min
• Respiratory rate >20b/min or PaC02 <32 mmHg
• WBC>12000/mm3 or <4000/mm3 or >10% immature
bands
.
64. When sepsis is accompanied by hypotension that is
refractory to volume infusion, the condition is called
Septic shock.
Early stages
Hyperdynamic or “warm” shock
Late stages
Hypodynamic or “cold” shock
Criteria
1. Sepsis- Sequential (sepsis-related) Organ Failure Assessment
(SOFA) score ≥2 above baseline values
2. Septic shock - vasopressor requirement to maintain a MAP≥
65 mmHg and a S.lactate >2 mmol/L in the absence of
hypovolaemia
66. NEUROGENIC SHOCK
Neurogenic shock is the interruption of autonomic
pathways leading to hypotension and bradycardia (and
hypothermia).
It is common in injuries involving cardiac sympathetics
(T2 –5) resulting in a decrease in systemic vascular
resistance, decreased inotropism, and increased
unopposed resting vagal tone.
CAUSES
• High cervical spinal cord injury (vertebral body #)
• Inadvertent cephalad migration of spinal anaesthesia
• Epidural hematoma or devastating head injury
67. PATHOPHYSIOLOGY
Initial- massive release of catecholamines- HR, BP
Followed by, fall in sympathetic tone- BP
When T2-T5 involved- vasodilation, inotropism, HR
68. PATHOPHYSIOLOGY
Loss of reflexes below the level of spinal cord injury
C/F- flaccid areflexia, hypotension
Gradual return of reflex activity when the reflex arcs
below redevelop
This is a complex process and a recent four-phase
classification to spinal shock has been postulated:
1. Areflexia (Days 0– 1)
2. Initial reflex return (Days 1–3)
3. Early hyperreflexia (Days 4–28)
4. Late hyperreflexia (1–12 months).
69. CLINICAL FEATURES
Alert and responsive-if head injuries are absent
Warm extremities above level of injury
Cool -below level of injury
Diaphragmatic breathing
Hypotension without obvious cause
Bradycardia
Priapism
Flaccid areflexia (e.g. in legs but tone in arms)
Loss of pain response below a level.
70. TREATMENT
Fluid resuscitation- with NS
Vasopressor support
Early vasopressor support has been advocated to ensure
adequate spinal cord perfusion pressure and reduce secondary
cord injury.
Supportive measures
Surgery
Stabilization, open or closed reduction, and surgical
decompression must be considered to relieve direct pressure
on the cord and prevent secondary injury
71. ANAPHYLACTIC SHOCK
‘‘a serious, generalized or systemic, allergic or
hypersensitivity reaction that can be life-threatening or
fatal’’
Ana-phylaxis means– (anti)-phylaxis, protection or
guarding.
Anaphylaxis is a potentially life-threatening systemic
allergic reaction involving one or more organ systems
occuring within seconds to minutes of exposure to the
anaphylactic trigger.
72. ANAPHYLACTIC SHOCK
Anaphylactic shock is an anamnestic response of an
individual to an antigen which is characterized by
1. Severe vasodilation
2. Bronchoconstriction
3. Pruritis
4. Increased vascular permeability
73. ETIOLOGY
Drugs
Blood products and vaccines
Diagnostic agents
Venom
Hormones
Extracts of allergens used for desensitization
Food
74. PATHOPHYSIOLOGY
EFFECTOR MOLECULES AND RECEPTORS
1. IgE mediated (with prior sensitization)
2. Non-IgE mediated reactions
3. Role of IgG and FcgRs
4. Role of complement
75. POTENTIAL EFFECTOR CELLS OF ANAPHYLAXIS
Mast cells – key cells
Basophils
Neutrophils
Monocytes and macrophages
Histamine
Platelets
PAF
CystLTs
Other mediators include prostaglandins, TNF-α
POTENTIAL MEDIATORS OF ANAPHYLAXIS
76.
77.
78. DIAGNOSIS
History
Signs and symptoms
Identify the specific cause
Serum biomarker – Histamine
Useful biomarker - S.tryptase
79. TREATMENT
Early recognition
First line – A B C
Patient position- upright
or sitting posture may
lead to the “empty heart
syndrome”
Second line- used to
treat anaphylaxis
refractory to the first-
line treatments or
associated with
complications
80. Drugs In Daily Anaesthetic Practice With Risk Of
Anaphylaxis
Local Anaesthetic- Lignocaine (preservative –
methyl paraben)
Muscle relaxants- Atracurium, rocuronium
IV induction agents- Propofol, Etomidate (egg
lecithin based)
Narcotics- Morphine
Analgesics- NSAIDS
Dextrans
Latex exposure
81. HYPOADRENAL SHOCK
Unrecognized adrenal insufficiency complicates the host
response to the stress induced by acute illness or major
surgery.
Etiology
Chronic administration of high dose of corticosteroids
Relative hypoadrenal state
Idiopathic atrophy-
• Etomidate induction
• Tuberculosis
• Metastatic disease
• B/L adrenal haemorrhage
• Amyloidosis
82. Clinical features: Loss of homeostasis- reduction in SVR,
hypovolemia, reduced CO.
Management:
ACTH stimulation test for diagnosis- may or may not be
consistent
Treatment
• Dexona 4mg - persistently hemodynamically unstable
patients. Dexona can be started empirically
• Hydrocortisone 100mg Q6hrly or Q8hrly
• Volume resuscitation and inotropic support
83.
84. CONCLUSION
As Anaesthesiologists and Intensivists, it is important to
understand the pathophysiology, recognise a patient in
shock and prompt treatment.
Rapid assessment with resuscitation
Source control ( Bleeding, Infection) – Highest priority
Regardless of source, the fundamental primary treatment
of shock remains recognition & stabilisation of
hemodynamics.
In trauma Arrival to on table time – very crucial
Practicing in a developing country, and in a tertiary care
hospital, we must be skillful in using minimal resources to
give the best possible outcome.
85. REFERENCES
Principles of Critical Care, Udwadia, 2nd edition
The ICU Book, Paul Marino, 4th edition
Harisson’s Principles of Internal Medicine, 20th edition
Tintinalli’s Emergency Medicine, A Comprehensive Study Guide, 8th
edition
Goldmann and Cecil, Textbook of Medicine, 25th edition
N Engl J Med 2018;378:370-379 DOI:10.1056/NEJMra1705649
Circulation. 2017;136:e232–e268. DOI:10.1161/CIR.0000000000000525
frca.uk.co
Continuing Education in Anaesthesia, Critical Care & Pain | Volume 13
Number 6 2013 doi:10.1093/bjaceaccp/mkt021
American Academy of Allergy, Asthma & Immunology
http://dx.doi.org/10.1016/j.jaci.2017.06.003
Ms Sharene Pascoe, Ms Joan Lynch 2007, Adult Trauma Clinical
Practice Guidelines, Management of Hypovolaemic Shock in the
Trauma Patient,NSW Institute of Trauma and Injury Management.
