shock

1. SHOCK

2. • What is shock?
• Shock is a state of circulatory insufficiency that creates
an imbalance between tissue oxygen supply (delivery)
and oxygen demand (consumption)
• resulting in end-organ dysfunction.
• Reduction in effective perfusion may be due to a local
or global delivery deficiency or utilization deficiency
with suboptimal substrate at the cellular or subcellular
level
SHOCK

3. • Types of shock
• Hypovolemic
• Cardiogenic
• Obstructive
• Distributive Septic, Neurogenic,
Anaphylactic
TYPES OF SHOCK

4. Stages of shock
•Initial
•Body compensatory mechanism
•Progression
•Irreversible

6. Hypoxia & acidosis
↓
Complement & neutrophil activation
↓
Free radical & cytokine release
↓
Injury to capillary endothelial cells
↓
Further activation of immune & coagulation systems
↓
Damage to endothelium with loss of integrity
↓
Leaky capillary endothelium
↓
Tissue edema & cellular hypoxia

7. CARDIOVASCULAR
PATHOPHYSIOLOGY
7
Shock
↓
↓ Preload & ↓ Afterload
↓
↑ sympathetic output
↓
catecholamine release from adrenal medulla
↓
↑ heart rate & contractility
venous and arterial vasoconstriction (Except in sepsis)

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

9. RENALPATHOPHYSIOLOGY
• Decreased renal blood flow
• RAS activation
• ↓ GFR + ↑ aldosterone & vasopressin
→ Oliguria
• Further vasoconstriction → ↑ sodium
& water retention → edema
• Toxic tubular injury & Tubular obstruction

10. ENDOCRINE PATHOPHYSIOLOGY
• Na+ & water retention  K+ & H+ lost
• Hypovolaemia  ADH
• Adrenergic drive  Norepinephrine
release
• Vasoconstriction
• ↑ glycogenolysis & ↑ gluconeogenesis
• ↓ Insulin release

11. CRH (Hypothalamus)
↓
ACTH (pituitary)
↓
Cortisol (Adrenal Cortex)
↓
Cortisol + Epinephrine + Glucagon  Catabolic state
↓
Gluconeogenesis & Insulin resistance
↓
Hyperglycemia, Muscle protein break down, lipolysis
ENDOCRINE PATHOPHYSIOLOGY

12. METABOLIC
DERANGEMENTS
• Anaerobic metabolism  Lactate
• ↑ Hepatic gluconeogenesis
• Hepatic lipogenesis  ↑ TG
• Protein catabolism → muscle
wasting

13. HYPOVOLAEMIC SHOCK

14. Definition
• A condition in which rapid fluid loss that results
in multiple organ failure due to inadequate
circulating volume and subsequent inadequate
perfusion.

15. • Hypovolemic shock is the most common type of
shock and is caused by insufficient circulating
volume.
• The normal blood volume per body weight of
adult is 7 %, whereas a child is 8-9%.
Hypovolemic Shock

16. Classification
HEMORRHAGIC SHOCK
• GI bleed
• Trauma
• Massive hemoptysis
• AAA rupture
• Ectopic pregnancy
• Post-partum bleeding
NON-HEMORRHAGIC
SHOCK
• Vomiting
• Diarrhea
• Bowel obstruction
• Pancreatitis
• Burns
• Environmental
(dehydration)

17. Hypovolemic Shock
• Heart pumps well, but not enough blood volume to
pump
MAP = CO x SVR
HR x Stroke volume
↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR
• Decreased Intravascular volume (Preload) leads to
Decreased Stroke Volume

19. Clinical
Sign

20. Management
• Restore oxygen delivery and repay oxygen debt
• Intravascular volume
• CO
• Hb

21. MANAGEMENT
HAEMORRHAGIC HYPOVOLEMIC
FLUID THERAPY
a) 1L of isotonic (0.9% NS or Hartmann’s),
continue until haemodynamic stable
(3L of fluid needed to raise 1L of intravascular
volume)
b) COLLOID or BLOOD PRODUCT
(PACKED CELL/SAFE O/FFP)
c) VASOPRESSOR – if not responding to
fluid
ADULT :
1-2L (10-30cc/kg) crystalloid
(further fluid rhesus with colloid or PC may needed)
IDENTIFY CAUSE & CONTROL BLEEDING IDENTIFY CAUSE
a) IV TRANEXAMIC ACID 1g stat & TDS
b) IV Nexium or pantoprazole 80mg stat
then, IVI infusion 8mg/h over 72H
c) Immobilisation
d) Early wound dressing/ compression

22. 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)

23. Hemorrhagic shock
• A condition of reduced tissue perfusion resulting in
the inadequate delivery of oxygen and nutrient that
are necessary for cellular function.
• Fluid resuscitation does not stop the bleeding. If the
bleeding doesn’t stop immediately, PUSH TO OT.
• Prior to surgery, if the LOW BP, transfuse IV fluids
and blood .
• If the BP is normal, don’t transfuse,the pressure
might dislodge the blood clots that spontaneous
stop the bleeding.

24. Investigations
• FBC- look for HcT and Hb
• BUSEC – look Acute Renal Failure, elevated urea can indicate
UGIB, Potassium, Sodium, Bicarb
• ABG
• Lactate
• Cardiac markers.
• ECG
• CXR
• GXM
• Capillary blood glucose
• UPT
• Blood cultures
• Abdominal USG
• ECHO

27. CARDIOGENIC
SHOCK

28. Definition
• Deterioration of tissues / cellular functions with
inadequate supply of oxygen & nutrients
secondary to failure of cardiac function.

29. • As a result of decreased myocardial
contractility and inadequate
systemic vasoconstriction from a
systemic inflammatory response to
extensive myocardial damage.

30. Pathophysiology
• Heart fails to pump blood out
MAP = CO x SVR
HR x Stroke Volume

31. Causes of cardiogenic shock
Myopathic Mechanical
Acute myocardial infarction
(most common)
Acute mitral regurgitation
Myocarditis Ventricular septal/aneurysm
rupture
Dilated cardiomyopathy Left ventricular
inflow/outflow tract
obstruction
Right ventricular failure Cardiac Arrthymia

33. Clinical Presentations
• Impaired circulation : tachycardia, delayed capillary refill,
hypotension, diaphoresis, poor peripheral pulses
• End organ dysfunction (e.g. decreased mental function and
urinary output)
• Jugular venous distension as evidence of RVF
• Pulmonary oedema from left ventricular dysfunction
• Loud murmurs may indicate valvular dysfunction
• Gallop (S3 heart sound) pathognomonic of congestive
heart failure

34. Specific Investigations
• ECG
• Echo
• CXR
• Serum BNP

35. Specific Management
Airway, Breathing, Circulation
• Endotracheal intubation and mechanical ventilation for
patient with excessive work of breathing
• High flow oxygen given via a mask to maintain SaO2 at
>90%
• Intravenous fluids to maintain adequate preload
Intravenous opioids (e.g. morphine 2-4mg)  to relieve
pain, induce sedation, block adrenergic discharge and lessen
cardiac stress

36. Specific Management
• Intravenous vasopressors  provide inotropic support to
increase perfusion
• To be used with caution  to avoid extreme heart rates
which may increase myocardial oxygen consumption,
increase infarct size and impair cardiac pump ability
• Examples : Dobutamine (drug of choice – improve cardiac
contractility), Dopamine, Digoxin
• Intra-aortic balloon pump recommended as a stabilising
measure and combined with thrombolytic therapy if
angiography and revascularization are not readily available.

37. Scenario
• 68-year-old male complaining of shortness of breath. His shortness of breath began after waking
six hours earlier and is progressively getting worse. Since lunch he has been unable to ambulate
without becoming significantly short of breath. He hasn’t been feeling great over the past several
days and has had a productive cough that has occasionally awoken him from sleep.
• History: HTN, previous MI (2002), hypothyroid
• Allergies: none
• Medications:Amlodipine, levothyroxine, warfarin
• Vitals: HR is 130, BP is 106/60, RR is 26/min, SpO2 is 90 percent, DXT-17, Temp- 38.5 C, and
lung sounds are bilateral crepitations up to mid zone.

39. SEPTIC SHOCK
• Sepsis : Life threatening organ dysfunction caused by
dysregulated host response to infection.
• Organ Dysfunction: Change in baseline Sequential
Organ Failure Assessment (SOFA) score
• Quick Sepsis-Related Organ Failure (qSOFA)  >2 :
SEPSIS
I. Hypotension : SBP <100 mmHg
II. Altered mental status : GCS <13
III. Tachypnoea: RR >22

40. • 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)

42. Sepsis : associated with vasodilation, capillary leakage & decreased effective circulating blood volume, reduced venous
return. Then, lead to impaired tissue perfusion and organ dysfunction
MANAGEMENT
FLUID RESUSCITATION IV CRSTALLOID 30cc/kg bolus (within 3H) (max 3-5L)
Reassess hemodynamic status to guide resuscitation
[Dynamic resuscitation markers (Passive leg raise test)]
Cautions in patients with limited cardiorespiratory reserve – fluid overload causing :
• Pulmonary oedema
• Hypoxemic respiratory failure
• Organ oedema
• Intra-abdominal hypertension
• Prolonged ICU stay & mechanical ventilation
VASOPRESSOR Target MAP (65 mmHg)
(Eg : Noradrenaline / Adrenaline)
ANTIMICROBIAL THERAPY ANTIMICROBIAL THERAPY
Broad-spectrum antibiotics
Anti-fungal (consider in) :
Total parenteral nutrition
Recent broad-spectrum antibiotic exposure
Perforated abdominal viscus
Immunocompromised
Clinical suspicious of fungal infection

43. • A 76-year-old obese Malay male with past medical history of hypertension ,chronic obstructive
pulmonary disease diabetes mellitus type II , atrial fibrillation , gastroesophageal reflux disorder,
and benign prostatic hypertrophy presented to the ED with acute-onset shortness of breath. On
initial examination, the patient was in respiratory distress, speaking in phrases, with diffuse
erythema and associated severe pruritus. He described an acute onset of these symptoms
approximately 30 minutes prior to arrival to the ED. On initial evaluation, he gave us a piece of
paper on which he had written “lactulose” implicating this as the new and only medication or
substance he had ingested in the three hours prior to presentation.
• At the time of arrival, the patient’s blood pressure (BP) was 177/143 millimeters of mercury
(mmHg), heart rate (HR) 163 beats per minute (bpm), respiratory rate (RR) 23 breaths per minute,
oxygen saturation of 93% on room air, weight 103 kilograms (kg). He was in acute respiratory
distress in tripod position, with an urticarial eruption on his trunk. Auscultation was significant for
inspiratory and expiratory wheezes in all lung fields. Oropharyngeal exam revealed an edematous
soft palate with a brawny texture and elevation of his tongue to the hard palate, with associated
difficulty tolerating his oral secretions.

45. Definition

46. • Only a trace amount of the trigger may be needed to
cause a severe reaction.
• Prescription and OTC medications.
• penicillin and NSAIDS  most common
• Venom of stinging insects
• Foods, especially high-protein foods
• Transfusion of blood.
• Substances such as latex (natural rubber).
• Dyes and contrast materials used during radiologic
procedures or tests.

47. Pathophysiology

49. Angioedema

50. Urticarial rash

51. Anaphylactic Shock
• Clinical diagnosis
• Look for exposure to drug, food, or insect bite.
• Lab investigations have no role.

52. Specific Management
• ABC’s
• Angioedema and respiratory compromise require
immediate intubation
• Vital signs, cardiac monitor, pulse oximetry.
• Set IV line, oxygen.

53. MANAGEMENT
• Allergic Reaction :
• IV Hydrocortisone 200mg / 4mg/kg (Paeds)
• IV Piriton 10mg / 0.1mg/kg (Paeds)
• IV Ranitidine 50mg
• Anaphylaxis :
• IV Hydrocortisone 200mg (Paeds 4mg/kg)
• IV Piriton 10mg (Paeds 0.1mg/kg)
• Neb Salbutamol (Wheezing/rhonci)
• IM Adrenaline 0.5mg (Paeds : 10mcg/kg) repeat every 5 minutes as needed
• Anaphylactic Shock :
• ABCDE
• IV Adrenaline 0.1mg (1:10000) slow bolus over 5-10mins (Paeds 0.01mg/kg)
• IVI Adrenaline 3mg in 50cc NS run at 3mls/Hour
• IM/ s/c Adrenaline: 0.5mg (1:1000) Adult / Paeds 0.01mg/kg
• IVD 1-2L Bolus
• IV Hydrocortisone 200mg
• IV Piriton 10mg
• IV Prednisolone 3mg

55. DEFINITION
•Obstruction to blood flow
around the circulation.
• e.g Pulmonary Embolism , cardiac tamponade
•Davidson Medicine
22nd Edition

56. OBSTRUCTIVE SHOCK
↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR

57. Obstructive shock has much in
common with cardiogenic shock
• Caused by mechanical
obstruction of blood
flow to and/or from the
heart
- something blocks
perfusion to the heart.
- Tension pneumothorax
- cardiac tamponade
- pulmonary embolism
Heart is working but there is a
block to the outflow
• Massive pulmonary embolism
• Aortic dissection
• Cardiac tamponade
• Tension pneumothorax
• Obstruction of venous return to
heart
• Vena cava syndrome - eg.
neoplasms, granulomatous
disease
• Sickle cell splenic sequestration

59. Features of obstructive
shock
•Chest pain
• Dyspnoea
• Orthopnoea
•Cold, clammy peripheries
•Signs of specific aetiology, eg.
Muffled heart sound, unilateral
hyperresonant lung fields.

60. Features of obstructive
shock
• Heart rate = high
• Central venous pressure = high
• Systemic vascular resistance =
high
• Mixed venous O2sat = low
• Cardiac output = low

61. • Tension pneumothorax
•  Increased pressure within the thoracic cavity blocks
the normal flow of blood to the heart
•  Immediate relief by needle thoracotomy followed by
definitive tube thoracotomy.
• Cardiac tamponade
•  Blood in the pericardium prevents blood from
entering the heart (venous return)
•  perform a FAST scan, obtain urgent cardiothoracic
consult and prepare for pericardiocentesis

62. Pulmonary Embolism
A portion of a venous
clot breaks off, travels
through the venous
system through the
right side of the heart,
and subsequently
enters a pulmonary

63. Clinical Approach - History
• Risk factors
• Symptoms
– Completely asymptomatic
– Acute dyspnoea
– Pleuritic chest pain
– Unexplained tachycardia
– Syncope/shock
– Cough, hemoptysis

64. Clinical approach – Physical
Examination
• Hypotension
• Elevated JVP

65. Investigation
Laboratory Imaging

66. Investigation - Lab
• If undetectable, it excludes
a diagnosis of PE
Serum d-
dimer
• low PaO2 and low SpO2
ABG
• Increase
ESR
• Increase
Serum LDH

67. Investigation - Imaging
• Radiological investigation of choice
• Blood clot appears as a filling defect in a contrast-
enhanced pulmonary artery. Sensitivity 90% and
specificity 95%
CT Pulmonary Artery of
Chest
• Normal or
classical findings of atelectasis, wedge shape lesio
n and pruning of pulmonary vessels
CXR
• Nonspecific (tachycardia) or
classical finding of S1, Q3, T3 and right strain p
attern including RBBB and RV hypertrophy
ECG
• Right side strain and in severe cases, blood clot
seen inside the RA, RV, RVOT and also in pulmonary
artery
Echocardiogram
• Homogeneous scintillation throughout the lung in
the perfusion portion rules out PE with 100%
sensitivity
V/Q scanning
• Performed to detect clot in pelvic or iliofemoral
veins
Compression US

68. CXR:
• Pleural effusion
• Cardiomegaly
• Atelectasis
• Hampton hump: shallow
wedge-shaped opacity in lung
periphery
• Westermark sign (in circle):
sharp pulmonary vessel with
distal hypoperfusion
• Palla’s sign (arrow): enlarged
right descending pulmonary
artery

69. Initial Management in ED
1. Utilize supplemental oxygen when
necessary to maintain adequate
pulse oximetry readings.
2. Administer intravenous crystalloid
fluids as needed to augment
preload and correct hypotension
3. Initiate initial anticoagulation
(LMWH favorable)
4. Systemic fibrinolytic therapy should
be considered for selected patients
with severe PE and no
contraindications.

70. Initial Management in ED
6. Surgical and suction thromboembolectomy
are options for patients with life-threatening
PE and contraindications to fibrinolysis. Open
surgical thromboembolectomy has high
mortality, but may be improved with early
and appropriate patient selection.
7. ICU admission when signs of circulatory
compromise are present or when
thrombolytic therapy is given and close
monitoring is needed

71. NONTRAUMATIC CARDIAC
TAMPONADE
• An increase in the amount of fluid within the
pericardial sac results in an increase in intrapericardial
pressure.
• The normal fibrocollagenous parietal pericardium has
elastic properties and stretches to accommodate
increases in intrapericardial fluid.
• If fluid continues to accumulate, intrapericardial
pressure rises to a level greater than that of the normal
filling pressures of the right heart chambers.
• When this occurs, ventricular filling is restricted and
results in cardiac tamponade.

72. Common Causes of Cardiac
Tamponade in Medical
(Nontrauma)Patients

73. Clinical Feature
• Symptoms are nonspecific, and patients most commonly complain of dyspnea at rest and with
exertion.
• Additional symptoms may be due to the underlying disease (e.g., uremia or tuberculous
pericarditis).
• Physical examination may reveal tachycardia and low systolic arterial blood pressure with a
narrow pulse pressure.
• Pulsus paradoxus may also be present. A paradoxical arterial pulse is said to be present when
the cardiac rhythm is regular and there are apparent dropped beats in the peripheral pulse
during inspiration.
• There is usually a<10 mm Hg decrease in systolic blood pressure during inspiration inthe
supine position.
• Pulsus paradoxus is not diagnostic of cardiac tamponade and may be noted in other
cardiopulmonary processes.
• In cardiac tamponade, the neck veins may be distended with an absent “y” descent.
• The apical impulse is indistinct or tapping in quality.
• Cardiac auscultation may reveal “distant” or soft heart sounds.
• Pulmonary rales are usually absent, and there may be right upper quadrant tenderness from
hepatic venous congestion.

74. Diagnosis
• The chest radiograph may or may not reveal an
enlarged cardiac silhouette because this finding
depends on the amount of intrapericardial fluid
accumulation.
• The ECG usually shows low-voltage QRS
complexes (<0.7 mV) and ST-segment
elevation (due to the inflammation of
the epicardium) with PR-segment
depression, as in pericarditis.

75. Echocardiography
• Diagnostic test of choice.
• In addition to a large pericardial fluid volume,
typical echocardiographic findings described in
cardiac tamponade:
• right atrial compression, RV diastolic collapse,
• abnormal respiratory variation in tricuspid and
mitral flow velocities
• dilated inferior vena cava with lack of inspiratory
collapse.

76. Treatment and Disposition
• Volume expansion with a bolus of normal saline
solution (500 to 1000 mL) will increase
intravascular volume, facilitate right heart filling,
and increase cardiac output and arterial pressure.
• However, it is a temporary measure.
• Pericardiocentesis is necessary for definitive
therapy and for specific diagnosis.

77. Tension Pneumothorax
• “one-way valve” air leak occurs
from the lung or through the chest
wall
• Air is forced into the pleural space
with no means of escape,
eventually collapsing the affected
lung
• mediastinum is displaced to the
opposite side, decreasing venous
return and compressing the
opposite lung
• Shock results from marked
decrease in venous return, causing

79. Signs and symptoms
– Chest pain
– Air hunger
– Tachypnea
– Respiratory distress
– Tachycardia
– Hypotension
– Tracheal deviation away from the side
of the injury
– Unilateral absence of breath sounds
– Elevated hemithorax without
respiratory movement
– Neck vein distention
– Cyanosis (late manifestation)

80. Diagnosis
• Arterial saturation should be
assessed using a pulse oximeter
and will be decreased when
tension pneumothorax is present
• Tension pneumothorax can be
diagnosed using an extended
FAST (eFAST) examination.

81. Management
• Tension pneumothorax requires
immediate decompression and may
be managed initially by rapidly
inserting a large over-the-needle
catheter into the pleural space
• Tube thoracostomy is
mandatory after needle
or finger decompression
of the chest
https://www.youtube.com/wa
tch?v=zrUASl8onPY

83. DEFINITION
•Major Brain or spinal injury
which distrupts brainstem
and neurogenic vasomotor
control.
• Davidson's Medicine
22nd edition

84. Neurogenic Shock
• It is a form of distributive shock
• Rarest form of shock
• Caused by sudden loss of sympathetic tone to
regions distal to the level of injury resulting in
vasodilation as well as restricting both reflex
tachycardia and vasoconstriction responses to
hypovolemia

86.  Occurs after acute spinal cord injury
 Sympathetic outflow is disrupted leaving unopposed
vagal tone
 Results in hypotension and bradycardia due to loss
of cardiac sympathetic tone.
 Warm skin due to dilatation of peripheral blood vessels
 Shock usually lasts from 1 to 3 weeks
 Any injury above T1 can disrupt the entire
sympathetic system
• Higher injuries = worse paralysis
Neurogenic Shock

87. Other Investigation
 CT of head/sinuses
 Lumbar puncture
 Wound cultures
 Acute abdominal series
 Abdominal/pelvic CT or US
 Cortisol level
 Fibrinogen, FDPs, D-dimer

88. Management
 Intravenous Fluid : Large volumes may be needed to restore
normal hemodynamics but care should be taken not to
overload as it may precipitate pulmonary edema. Monitor the
urinary output with an indwelling urinary catheter.
 Inotropic Support: Dopamine is often used
 Atropine: Increase Heart Rate
 Vasopressors: If hypotension remains refractory to treatment
**Urgent Orthopedic / Neurosurgical consult/ referal

89. The end point of resuscitation in
shock therapy
• There is no obvious end point to resuscitation as the process is dynamic.
The mainstay is to ensure the cause of shock is identified and manage
adequately or condition reversed or improved.
• The goal of trauma resuscitation and shock therapy is to ensure the ABCDE
is adequately managed and goals of resuscitation are achieved.
• Parameters to consider include:
• 1. Mental status improved
• 2. Vital signs normalized
• 3. Perfusion improved
• 4. A urine output of greater than 0.5 ml/kg/h
• 5. CVP reading of 8-12 mmHg
• 6. Mean Arterial pressure of 65-95 mmHg.
• 7. ABG improved
• 8. Lactate clearance.

90. 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

91. Reference

92. Thank YOU