Pathopysiology and management

1. Presented By: Dr R Kumar Unit
Ankit Srivastava & Shakeel Jawed

2. SHOCK
Shock is a systemic state of low tissue
perfusion which is inadequate for normal
cellular respiration.With insufficient delivery
of oxygen and glucose, cells switch from
aerobic to anaerobic metabolism. If perfusion
is not restored in a timely fashion, cell
death ensues.

3. The term shock appears to have
been first used in 1743 in a
translation of the French treatise
of Henri Francois Le
Dranregarding battlefield
wounds.

4.  “Shock is the
manifestation
of the rude
unhinging of
the machinery
of life”
4

5.  The state in which profound
and widespread reduction of
effective tissue perfusion
leads to first reversible ,and
then if prolonged, leads to
irreversible cellular injury

6. • Ambroise Paré (1510) – Fluids to injured patients
• ‘Shock’ – 1743 – act of impact/ collision
• Guthrie (1815) – described physiological
instability
• Crile (1899) – Importance of measuring BP
• Claude Bernard – Milieu intérieur
• Walter B. Cannon – Homeostasis
• WW I – Disturbance of nervous system
• Alfred Blalock (1934) – 4 categories of shock
• Carl JohnWiggers (1950) –Wiggers prep
6

9.  PUMP- Heart
 PIPES- Vessels
 FLUID- Blood
 Pump Failure : cardiogenic shock,obstructive
 Pipe Failure : distributive shock
 Loss of Fluid : hypovolemic shock
How can Perfusion fail??

11.  Hypoxia
↓
 Anaerobic metabolism
↓
 Lactic acidosis
↓
 Cell wall damage
↓
 Sodium and calcium enter the cell
↓
 Potassium leaks out of the cell
↓
 Causes hyperkalaemia, hyponatraemia and
hypocalcaemia
↓
 Intracellular lysosomes break down releasing powerful
enzymes which destroy own cell

14. Hemorrhagic
trauma
Bleeding
disorder
GU/GI
bleeding
Non
Hemorrhagic
. Poor fluid
intake:
dehydration
Excessive fluid loss
: vomiting,
diarrhoea, urinary
loss (eg. diabetes),
evaporation,
. ‘third-spacing’
spaces,eg bowel
obstruction or
pancreatitis.
Reduced circulating blood volume

18.  . Myocardial
Infarction
Cardiac
dysrhythmias
Valvular
heart disease
Blunt
myocardial
injury
cardiomyo
pathy

22. Tension
Pneumothorax
Cardiac
tampona
de
Pulmonary
embolism
• Herniation
Of the gut
through
Diaphraga
m

25.  CAUSES Septic Shock
Neurog
enic
Shock
DRUG /Toxin
Induced Shock
Anaphy
lactic
Shock

26.  A type of distributive shock that results
from widespread systemic allergic
reaction to an antigen .
 There is vasodilation due to histamine
release
 This TYPE I hypersensitive reaction is LIFE
THREATENING

28.  A clinical response arising
from a nonspecific insult,
with 2 of the following:
 T >38oC or <36oC
 HR >90 beats/min
 RR >20/min
 WBC >12,000/mm3 or
<4,000/mm3 or >10%
bands
SIRS = systemic inflammatory
response syndrome
SIRS with a
presumed
or confirmed
infectious
process
SepsisSIRS
Severe
Sepsis
Septic
Shock
Sepsis with
organ failure
Refractory
hypotension

30.  Endocrine shock may present as a
complication of
1.Hypovolemic shock
2.Cardiogenic shock
3.Distributive shock
 Causes:
1.Hypo/ Hyperthyoidism
2. Adrenal Insufficiency

31. HR Strok vol CO MAP PCWP SVR CVP
HYPOVOLUMIC INC DEC DEC DEC DEC INC DEC
CARDIOGENIC INC DEC DEC DEC INC INC INC
OBSTRUCTIVE INC DEC DEC DEC INC INC INC
DISTRIBUTIVE INC INC INC DEC DEC DEC DEC
SEPTIC
(HYPERDYNAMIC
)
INC INC INC DEC DEC DEC INC
SEPTIC
(HYPODYNAMIC)
INC DEC DEC DEC INC INC DEC
NEUROGENIC DEC NO CHN DEC DEC DEC DEC DEC
ANAPHYLACTIC INC INC DEC DEC DEC DEC DEC

32. 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

35.  History
 Physical examination
 Laboratory Investigations
 Other investigations
 Treat the Shock - Start treatment as soon as
you suspect Pre-shock or Shock
 Monitor

36.  Trauma?
 Pregnant?
 Acute abdominal pain?
 Vomiting or Diarrhea?
 Hematochezia or hematemesis?
 Fever? Focus of infection?
 Chest pain?

37.  Vitals - HR, BP,Temperature, Respiratory
rate, Oxygen Saturation
 Random blood sugar
 Weight in children
 In a patient with normal level of
consciousness - Physical exam can be
directed to the history

38.  In a patient with abnormal level of
consciousness
 Primary survey
 Cardiovascular (murmurs, JVP, muffled heart
sounds)
 Respiratory exam (crackles, wheezes),
 Abdominal exam
 Rectal and vaginal exam
 Skin and mucous membranes
 Neurologic examination

42.  CBC, Electrolytes, Creatinine/BUN, glucose
 ABG
 Lactate
 Random blood sugar
 Liver funtion test
 +/- Cardiac Enzymes
 Blood Cultures - from two different sites
 +/- Cross Match

43.  ECG
 Urinalysis
 CXR
 +/- Echo
 +/- FAST(focused abdominal sonography for
trauma)

44. • Do you remember
how to quickly
estimate blood
pressure by pulse?
• If you palpate a pulse,
you know SBP is at
least this number
60
70
80
90

45. • ABCDE
• Airway
• control work of Breathing
• optimize Circulation
• assure adequate oxygen Delivery
• achieve End points of resuscitation

46. • Determine need for intubation but
remember: intubation can worsen
hypotension
• Sedatives can lower blood pressure
• Positive pressure ventilation decreases
preload
• May need volume resuscitation prior to
intubation to avoid hemodynamic
collapse

47. • Respiratory muscles consume a significant
amount of oxygen
• Tachypnea can contribute to lactic acidosis
• Mechanical ventilation and sedation decrease
WOB and improves survival

48. • Isotonic crystalloids
• Titrated to:
• CVP 8-12 mm Hg
• Urine output 0.5 ml/kg/hr (30 ml/hr)
• Improving heart rate
• May require 4-6 L of fluids
• No outcome benefit from colloids

49. • Decrease oxygen demands
• Provide analgesia and anxiolytics to relax
muscles and avoid shivering
• Maintain arterial oxygen saturation/content
• Give supplemental oxygen
• Maintain Hemoglobin > 10 g/dL
• Serial lactate levels or central venous
oxygen saturations to assess tissue oxygen
extraction

50. • Goal of resuscitation is to maximize survival
and minimize morbidity
• Use objective hemodynamic and physiologic
values to guide therapy
• Goal directed approach
• Urine output > 0.5 mL/kg/hr
• CVP 8-12 mmHg
• MAP 65 to 90 mmHg
• Central venous oxygen concentration > 70%

51.  AIM:To restore cardiac filling pressure promptly and
adequately without inducing pulmonary edema.
Measures:
1. Arresting ongoing blood loss.
2. Restoration of blood volume.
3. Correction of metabolic acidosis
Arresting ongoing blood loss:
 External haemorrage by pressure elevation and tourniquet.
 Internal haemorrhage by immediate surgical exploration.
Restoration of circulating blood volume:
Start two large bore I.V. cannula,
Debate still exists over the type, amount and rate of infusion of
fluids.
Fluid challenge test is the guideline for rate of infusion.

53.  Three steps:
 1. Initial stabilization
 2. Evaluation of the patient
 3. Definitive therapy

54.  1. Establishment of ventilation and
oxygenation to maintain PaO2> 70 mm Hg.
 2. Restore MAP > 70 mm Hg with volume
correction and vasopressors.
 3.Treatment of pain, arrhythmias and acid
base abnormality.

55.  Brief history, physical examination and
investigations.
 ECG-look for ischemic changes, cardiac
enzymes
 Cardiac filling pressure – CVP, PCWP, LVEDP
 Chest x-ray, ABG
 2D echo for ventricular function
 Arterial O2 saturation
 Starling function curve.

56.  Definitive therapy
 Goals of treatment
1. CI -4.5 l/min/ m2 (N – 3.0 – 3.4 l/min /m2).
2. DO2- 600 ml/min/ m2 (N – 480 – 600 ml/min
/m2)
3. VO2 – 140 – 180 ml/min /m2 (N – 130 – 160
ml/min/ m2)
Achieved by,
 1. Pharmacological support and / or
 2. Surgical intervention

57. 1)
Pharmacological support:
 Aimed at – increase C.O., improving coronary blood flow and decrease
transudation of fluid into the lung.
 Done by – modifying preload, after load and by increase inotropic
function of the myocardium.
Reduction in preload (diuretics):
 Decrease volume where excusive preload exists.
 Over use may result in organ hypoperfusion and renal failure.
 Loop diuretics
Improving myocardial contractility (inotropes):
 Inotropes are indicated where preload is optimal but low cardiac output
and
 hypotension exists.
 Sympathomimetic amines are potent inotropes which act via a and b
adrenergic
receptors.

59.  II. Surgical intervention:
 IABP
 Angioplasty
 CABG
 Cardiac transplant.

60. 60

61. Initial Resuscitation and Reverse the
underlying cause
Hemodynamic Support and Adjunctive
Therapy
SupportiveTherapy of Severe Sepsis
61

62.  A. Initial Resuscitation
 B. Screening for Sepsis and Performance Improvement
 C. Diagnosis
 D. AntimicrobialTherapy
 E. Source Control
 F. Infection Prevention
62

63.  Resuscitation of patients with sepsis- induced tissue
 Early resuscitation is the key
 Hypoperfusion
defined as hypotension persisting after initial fluid challenge or
blood lactate concentration ≥ 4 mmol/L
 EGDT (first 6 hrs of resuscitation)
 a) CVP 8–12 mm Hg
 b) MAP ≥ 65 mm Hg
 c) Urine output ≥ 0.5 mL/kg/hr
 d) Scvo2 or Svo2 70% or 65%, respectively
63

64.  Hypotension despite of fluid resuscitation;
 Systemic vasopressor I/d
 First line: Norepinephrine or dopamine
 If dopamine fail to increasrease MAP > 60mm
Hg , if excessive tachycardia or tachyarryhmia
norepinephrine should be used.

65.  As 2nd line may be helpful
 Inc MAP n SVR
 Considered in patient refractory to inotoric
agent n have CO > 3.5 l/min/m2

66.  Routine screening of seriously ill patients for severe sepsis to
 increase the early identification of sepsis
 allow implementation of early sepsis therapy
 Performance improvement efforts to improve patient
outcomes and decrease sepsis-related mortality.
66

67.  Cultures
 Imaging studies
67

68.  Initial empiric anti-infective therapy
 Broad spectrum
 Anti fungals
 Reassessed daily for potential de-escalation
 Combination empiric therapy
 Duration & De-escalation
68

69.  Hydrocortisone only to those patient
unresponsive to fluid resuscitation and
vasopressors
 Hydrocortisone drug of choice

70.  Intervention for source control within the first 12 hr of
diagnosis.
70

72. 72

73.  Diagnosis
Diagnosis is clinical
Chest X-Ray
Echocardiography
Pericardiocentesis
Treatment of the cause
73

74. TENSION
PNEUMOTHORAX
CARDIAC
TAMPONADE
PULMONARY
EMBOLISM
Sterile needle in 2nd
inter coastal space; tube
thoracostomy
Pericardiocentesis
Heparin infusion with
or without tPA

75. 75

76.  Diagnosis:
Hypotension with bradycardia
Warm extremities
Motor and sensory deficits
Radiographic evidence of vertebral fracture
76

77.  Treatment
Fluid resuscitation
Ionotropic support
Operative attempt to stabilise the vertebral
fracture.
77

78. 78