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
7.
8.
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??
10.
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
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
27.
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
29.
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
33.
34.
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
39.
40.
41.
42. CBC, Electrolytes, Creatinine/BUN, glucose
ABG
Lactate
Random blood sugar
Liver funtion test
+/- Cardiac Enzymes
Blood Cultures - from two different sites
+/- Cross Match
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.
52.
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.
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.
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