6. Hypovolemic Shock
■ Caused by decreased preload due to intravascular volume loss:
I. Haemorrhagic trauma
II. GI bleed
III. Fractures (Long bones)
IV. Fluid loss (diarrhoea, vomiting, burns)
8. Clinical Features
Clinical Features Why ?
Hypotension • BP may not fall until 30 – 40% blood loss
• BP often maintained by release of
catecholamines (Increased the Systemic
vascular resistance)
Tachycardia • Reduced CO results in sympathetic activation
• Via Arterial Baroreceptors
• Causes Increased in HR (CO = HR x SV)
Tachypnea • Hypoxia
• Respiratory compensation for Metabolic
Acidosis
Decreased Conscious Level • Decreased cerebral perfusion
Decreased Urine Output • Decreased renal perfusion
Cold Peripheries / Sweating • Vasoconstriction of cutaneous, muscle and
visceral circulation
• Preserved blood flow to heart, kidney and
brain
9. Acid/base category would be
expected.
■ Lactic acidosis , considered a type of metabolic acidosis, is a physiological
condition characterized by low pH in body tissues and blood (acidosis)
accompanied by the buildup of lactate.
■ Lactic acidosis is characterized by lactate levels >5
mmol/L and serum pH <7.35
■ Type A lactic acidosis is the most common type of lactic
acidosis in hypovolemic shock
10.
11.
12. CCTVR (CRT, Colour, Temp, Volume, PR) + BP, JVP
CLINICAL APPROACH TO SHOCK
■ A – Establish patent airway
■ B – Ensure adequate ventilation, O2 support, SpO2>95%
■ C – Circulation control – direct pressure over bleed site, 2 large bore
cannula, adequate fluid resuscitation and vasopressor drugs. Blood
remains the ideal resuscitative fluid in haemorrhagic case
■ D – Neurological exam and GCS
■ E – Exposure
13. SHOCK INDEX
■ The shock index (SI) is an indicator of the
severity of hypovolemic shock and is
calculated by dividing the heart rate (HR)
by systolic blood pressure (SBP)
■ It serves to predict the mortality, need for
blood transfusion, or necessity of
intensive care unit admission among
patients with trauma , postpartum
haemorrhage , acute myocardial
infarction , stroke, sepsis
■ The accepted value of shock index
ranges from 0.5 to 0.7
14. RUSH PROTOCOL/FAST SCAN
■ Rapid Ultrasound for Shock and
Hypotension
■ Focused Assestment with
Sonography for Trauma
15. MANAGEMENT
HAEMORRHAGIC HYPOVOLEMIC
FLUID THERAPY
a) 1L of isotonic (0.9% NS ),
continue until haemodynamic stable
(3L of fluid needed to raise 1L of intravascular
volume)
b) BLOOD PRODUCT
(PACKED CELL / SAFE O / FFP)
ADULT :
(20-30cc/kg) crystalloid
(further fluid resus with colloid or PC may needed)
PAEDIATRIC :
(Severe dehydration)
20cc/kg bolus 0.9% NaCl
IDENTIFY CAUSE & CONTROL BLEEDING IDENTIFY CAUSE
a) IV TRANEXAMIC ACID 1g stat & TDS
b) IV Pantoprazole 80mg stat then, IVI infusion
8mg/h over 72H
16.
17. Initial management of Haemorrhagic
shock
■ Vascular line access- minimum of 16-gauge in adult
■ Administer an initial warmed fluid bolus of isotonic fluids
– 1 L bolus for adults
– 20mL/kg for paeds (weight less than 40kg)
■ Early resuscitation with blood and blood products in Class III and IV
■ Low ratio of packed cell to plasma to platelet to prevent coagulopathy and
thrombocytopenia
– 1:1:1 = 1 packed cell: 1 FFP: 1 Platelet
■ Massive transfusion
■ Coagulopathy
18. Evaluation to initial therapy
■ General – Improvement in HR, BP, PR, GCS and peripheral perfusion
■ Urine output – CBD for urine output monitoring
i - Adult - Aim at least 0.5cc/kg/H
Ii - Paeds - Aim at least 1.0cc/kg/H (>2y.o.)
- Aim at least 2.0cc/kg/H (<2y.o.)
■ Blood gas + Lactate – Improvement in pH, HCO3 and lactate level may indicate
response to therapy
21. Cardiogenic Shock
■ Caused as a result of cardiac pump failure which lead to reduced cardiac output:
CAUSES :
I. Myocardial infarction
II. Arrhythmias (Tachyarrythmia, bradyarrythmia)
III. Mechanical (structural) abnormalities (valvular
defect)
IV.Dilated Cardiomyopathy
23. DIAGNOSTIC
CRITERIA
HYPOTENSION
- Systolic BP <90mmHg
- Vasopressors required to achieve a blood pressure
>90mmHg
SIGNS OF IMPAIRED ORGAN PERFUSION (at least one of the
following)
- Altered mental status
- Cold & clammy skin
- Oliguria
- Increased serum lactate levels
Evidence of left ventricular failure: pulmonary edema,
wheezing, frothy sputum
31. Obstructive Shock
■ Obstruction of the outflow due to impaired cardiac
filling and excessive afterload:
I. Tension Pneumothorax
II. Cardiac tamponade
III. Pulmonary embolism
33. TENSION PNEUMOTHORAX
■Air is forced to pleural space without escape due to flap valve mechanism causing
collapse of the affected lung
■This limits RV filling by obstruction of venous return
■Mediastinum shifted to opposite side
■Symptoms: Chest pain, SOB
■Signs: Hypotension
Tachycardia
Respiratory distress
Distended neck vein (Can be present in HF patient)
Trachea deviated to opposite side -> unequal chest rise
Percussion: Hyper resonance
Auscultation: Reduced breath sound
35. CARDIAC TAMPONADE
■ Compression of heart by accumulation of fluid in pericardial sac
■ Causes impaired diastolic filling of RV
■ Results in reduced cardiac output & reduced blood flow to heart
36.
37. CARDIAC TAMPONADE
■ Treatment
Rapid evacuation of pericardial space
Performed through an USG guided
Pericardiocentesis (temporizing measure)
Three main approaches can be used for
pericardiocentesis: the apical, the
subcostal or the parasternal approach.
Open Thoracotomy (definitive
treatment)
38. Place of Puncture Description Disadvantages Advantages
Apical The needle insertion site
is 1-2 cm lateral to the
apex beat within the fifth,
sixth or seventh
intercostal space.
Advance the needle over
the superior border of the
rib to avoid intercostal
nerves and vessels.
Risk of ventricular
puncture due to the
proximity to the left
ventricle.
Increased risk for
pneumothorax for the
proximity to the left pleural
space.
The thicker left ventricle
wall is more likely to self-
seal after puncture.
Due to ultrasound not
penetrating air, using
echocardiographic
guidance ensures
avoidance of the lung.
The path to reach the
pericardium is shorter.
Parasternal The needle insertion site
is in the fifth left
intercostal space close to
the sternal margin.
Advance the needle
perpendicular to the skin
(at the level of the cardiac
notch of the left lung).
Risk of pneumothorax and
puncture of the internal
thoracic vessels (if the
needle is inserted more
than 1 cm laterally).
Echocardiographic
guidance, also with phase
array probe, provides a
good visualisation of
pericardial structures.
Subxiphoid The needle insertion site
is between the
xiphisternum and left
costal margin. Once
beneath the cartilage
cage, lower the needle to
a 15-to-30-degree angle,
with the abdominal wall
directed towards the left
shoulder.
A steeper angle may enter
the peritoneal cavity, and
a medial direction
increases the risk of right
atrial puncture. In some
cases, the left liver lobe
may be transversed
intentionally if an
alternative site is not
available.
The path to reach the fluid
Lower risk of
pneumothorax.
39. Pulmonary Embolism
■ Blockage in one of pulmonary arteries in lungs by thrombus
• Symptoms : SOB, chest pain, haemoptysis, presyncope or syncope
■ Ix:
– ECG: usually sinus tachycardia
– Massive PE: S1Q3T3 pattern, RBBB
– CXR: usually clear
– ECHO: RV strain pattern
– D-Dimers
– Gold Standard: CTPA
• Treatment: Thrombolytic therapy
40.
41. PERC rule : The pulmonary embolism rule out criteria (low
and moderate risk)
1. Age <50 years
2. Heart rate <100 bpm
3. Oxyhemoglobin saturation ≥95%
4. No hemoptysis
5. No estrogen use
6. No prior DVT or PE
7. No unilateral leg swelling
8. No surgery/trauma requiring hospitalization within the prior four weeks
■In patients who fulfill all eight criteria, the likelihood of PE is low and no further testing is
required.
47. SEPTIC SHOCK
■ Sepsis : Life threatening organ dysfunction caused by dysregulated host response
to infection.
■ Screening
Quick Sepsis - Related Organ Failure (qSOFA) >2 : suggest poor outcome, not
used to diagnose
I. Hypotension : SBP <100 mmHg
II. Altered mental status : GCS <15
III. Tachypnoea: RR >22
48. 1) SIRS :
T >38’ or <36’
RR >20
HR >90
TWC >12,000 or <4,000
2) SEPSIS = 2 SIRS CRITERIA + CONFIRMED/SUSPECTED INFECTION
3) SEVERE SEPSIS :
Signs of end organ damage
Hypotension <90mmHg
Lactate acidosis
4) SEPTIC SHOCK :
- SEVERE SEPSIS + PERSISTENT HYPOTENSION DESPITE
ADEQUATE FLUID RESUSCITATION
SIRS AND SEPSIS
CRITERIA
1) SIRS :
T >38’ or <36’
RR >20
HR >90
TWC >12,000 or <4,000
pCO2 <32mmHg
2) SEPSIS = 2 SIRS CRITERIA + CONFIRMED/SUSPECTED
INFECTION
3) SEPTIC SHOCK :
- SEVERE SEPSIS + PERSISTENT
■ Signs of end organ damage
■ Hypotension <90mmHg
■ Lactate >4
49. ■ Serum lactate
– High level is indicative of
tissue hypoxia
– If initially it is >2mmol/L,
it has to be repeated
within 2-4hr to guide
resuscitation
■ Blood culture and
sensitivity
– In order to optimize
identification of
pathogens and improve
clinical outcome
50. ■ Septic Shock :
- Subset in sepsis circulatory and cellular/metabolic abnormalities are profound enough to
increase mortality :
Persistent hypotension require vasopressor to maintain MAP >65mmHg
Serum Lactate >2mmol/L despite adequate fluid resuscitation
Septic shock presents two phases:
An early warm phase, characterized by
– normal or increased cardiac output and central venous saturation
– low peripheral vascular resistance, wide pulse pressure
– bounding pulse, brisk capillary refill (< 3 sec)
A late cold phase, characterized by
– low cardiac output and central venous saturation,
– high peripheral vascular resistance, narrow pulse pressure,
– weak pulse, delayed capillary refill (> 5 sec)
51. Sepsis : associated with vasodilation, capillary leakage & decreased effective circulating blood volume, reduced
venous return.
WHICH Then, lead to impaired tissue perfusion and organ dysfunction
MANAGEMENT
FLUID RESUSCITATION IV CRYSTALLOID 30cc/kg bolus (tailored individually)
Reassess hemodynamic status to guide resuscitation
VASOPRESSOR Target MAP (65 mmHg)
- Noradrenaline -1st line agent
- Adrenaline
- Dopamine
ANTIMICROBIAL
THERAPY
EARLY ADMINISTRATION OF ANTIBIOTICS WITHIN 1H OF
RECOGNITION
Broad-spectrum antibiotics
Anti-fungal (consider in) :
Clinical suspicious of fungal infection
Total parenteral nutrition
Recent broad-spectrum antibiotic exposure
Perforated abdominal viscus
Immunocompromised
52. Neurogenic shock
■ Loss of sympathetic tone cause unopposed parasympathetic activity which
lead to massive vasodilatation in venous vasculature due to spinal cord injury
above T6
■ Causes:
I. Injury to cervical and upper thoracic spinal cord
II. Regional anaesthesia
III. Severe brainstem injury
■ Clinical:
I. Bradycardia
II. Hypotension
III. Warm and flushed skin (peripheral vasodilatation)
53. ASIA Chart
■ 2 components : MOTOR & SENSORY
■ To determine the level of neurological deficit in spinal cord injury
■ To determine the type of spinal cord injury: COMPLETE or INCOMPLETE
54.
55.
56. MANAGEMENT
■ A : Airway control with cervical spinal immobilization
– Need for intubation:
■ Tetraplegia
■ Resp distress: weak cough, shallow breathing
■ Diaphragmatic impairment
■ LOC
■ B : Secure breathing and ventilation
■ C : Need to rule ot haemorrhage as causes of hypotension
– Adequate circulation
– IV fluid bolus
– Inotropic agents, aim MAP >70mm Hg for spinal cord perfusion,
noradrenaline
57. Cont.
■ D: Complete neurological examination
Back:step deformity, hematoma, open fracture at the
back
Per rectal examination
ASIA charting
■ E: Keep warm
■ Early transfer to spinal unit
58. Anaphylactic shock
■ Allergic reaction immune system overreacts to a harmless substance
known as an allergen.
■ Anaphylaxis
o Rapid developing, severe, life threatening systemic hypersensitivity reaction
o Involve more than one systems
o Airway: Pharyngeal or laryngeal edema
o Breathing: bronchospasm
o Circulation: hypotension/tachycardia
o And usually associated with skin & mucosal changes: urticaria,
angioedema, erythema multiforme
■ Anaphylactic Shock
o Anaphylaxis + Shock
61. Anaphylaxis
Ig-E mediated Non-Ig-E mediated
* Insect stings, and foods *Opioids, vancomycin,
blood products,
Sensitizing antigen elicits an IgE
antibody response in susceptible
individuals
Antigen-specific IgE ab binds to
mast cells and basophils
Subsequent exposure to sensitizing
antigen causes cross-linking of cell-
bound IgE
Mast cells and basophils degranulation
Pathophysiology of anaphylaxis
Activation of complement cascade
Byproducts of the cascade (c3a, c4a, c5a
are known as anaphylatoxins
Cause mast cells or basophils degranulation
Preformed histamines, leukotrienes,
prostaglandins and platelet activating
factors(PAF) are released
62. Clinical Feature
■ Early:
– Sensation of warmth and itchiness
– Anxiety and panic
■ Progressive:
– Erythematous / urticarial rash
– Edema of face and neck
■ Severe:
– Hypotension
– Bronchospasm
– Arrythmias
63. Management
■ Stop trigger
■ A: maintain airway patency, consider intubation if present of airway edema
■ B: oxygen supply, nebulization if bronchospasm
■ C: IM Adrenaline 0.01mg/kg to maximum 0.3-0.5mg (First Line Treatment)
– If persistent hypotension/resp distress, repeat repeat IM adrenaline 0.5mg after 5 mins
– If still persistent, start adrenaline infusion 0.1-5.0mcg/kg/min
■ IV hydrocortisone 4mg/kg
■ Antihistamine: IV piriton
■ H2 blocker: IV Ranitidine
■ IV glucagon 1mg every 5 min in pt on b-blocker with refractory hypotension with adrenaline
and fluids
64. MANAGEMENT
■ Allergic Reaction :
– IV Hydrocortisone 200mg / 4mg/kg
– IV Piriton 10mg / 0.1mg/kg (Paeds)
■ Anaphylaxis :
– IV Hydrocortisone 200mg
– IV Piriton 10mg (Paeds 0.1mg/kg)
– Neb Salbutamol (bronchospasm)
– IM Adrenaline 0.5mg (Paeds : 0.01mg/kg) repeat every 5 minutes as needed
■ Anaphylactic Shock :
– ABCDE
– IM Adrenaline: 0.5mg (1:1000) Adult / Paeds 0.01mg/kg
– IVI Adrenaline 0.1-5.0 mcg/kg/min
– IVD tailored to patient 10cc/20cc/30cc rapid bolus over 1H
– IV Hydrocortisone 200mg
– IV Piriton 10mg
Cardiac index : cardiac output per square meter of body surface
Immediate hypersensitivity reaction (Type I), mediated by interaction of IgE on mast call and basophils triggers release of histamine, leukotrienes, and other mediators that cause diffuse smooth muscle contraction (eg, resulting in bronchoconstriction, vomiting, or diarrhea) and vasodilation with plasma leakage (eg, resulting in urticaria or angioedema).
